Category: Specialists-Cardiology

What does a normal or abnormal treadmill test mean?

TREADMILL testing is a common modality used by many doctors to screen for heart artery disease. For the couch potatoes who are suddenly fired up to become a paragon of fitness, current guidelines recommend that it will be wise for relatively inactive older men to undergo a treadmill stress test before embarking on a vigorous exercise regime. If the treadmill test result appears normal, does that mean that you do not have heart artery disease and you will not get a heart attack? If the test result is abnormal, does it mean that you have significant heart artery disease?

What is a treadmill stress test?

The treadmill stress test, though a commonly used screening test by doctors, has many limitations, especially for women. Patients are hooked up to a monitor which records the electrical pattern of the heart – also known as an electrocardiogram (ECG) – and walk on a treadmill machine which increases in speed and incline every few minutes according to the preset protocol. During the test, doctors look for changes in the ECG to screen for heart artery disease.

Treadmill test in women

Research from the last decade has revealed gender differences in heart disease. American Heart Association statistics have shown that 64 per cent of women who died suddenly from heart disease did not have classic warning symptoms, versus 50 per cent of men.

Moreover, 38 per cent of women died within one year following a heart attack, versus 25 per cent of men. Hence, there is a need to detect underlying heart artery disease in women. Although treadmill testing is widely used, the pitfalls of this method need to be understood.

Women are more likely to have baseline ECG changes even before they start walking on the treadmill, making interpretation of ECG changes with exercise difficult. They are also more likely to have more abnormal ECG changes with exercise testing, even in the absence of significant blockage of the heart arteries.

The situation is made even more perplexing by trial data, which shows no relationship between ST-segment depression with exercise stress testing and death – heart-related or otherwise.

The timing of the treadmill appears to affect the result as well. In pre-menopausal women with no significant heart artery disease, the presence of ST-segment depression during exercise appears to vary with the menstrual cycle. Exercise ST depression is more frequently observed in the luteal phase of the menstrual cycle – the run-up to a woman’s period starting from ovulation – than in the late follicular phase, which is the period leading up to ovulation.

Post-menopausal women receiving oral oestrogen therapy are more likely to have exercise-induced ST-segment depression with normal coronary angiograms than their sisters who are not on oestrogen replacement.

In a 2017 publication in the International Journal of Cardiology on the use of treadmill testing to detect coronary artery disease in Chinese women, treadmill testing had a sensitivity of about 80 per cent. When comparing post-menopausal women with pre-menopausal women, the specificity was 68 per cent versus 32 per cent. This means that for every 100 women with significant coronary artery disease, treadmill test results are abnormal in 80. It also means that for every 100 pre-menopausal women with an abnormal treadmill test, only 32 have significant coronary artery disease – which means that there is a high incidence of a false positive result in pre-menopausal women undergoing treadmill testing.

Accuracy of treadmill testing

The sensitivity and specificity of treadmill stress testing differs depending on the patient cohort, that is, whether there is a low prevalence or high prevalence of heart artery disease in the patient cohort.

In an early 1977 study published in Circulation journal looking at treadmill testing of patients who have documented coronary artery disease and had undergone heart artery bypass graft surgery, treadmill testing showed a high specificity of 91 per cent but had a low sensitivity of 32 per cent (in patients with residual heart artery disease which was not bypassed) .

In a low-prevalence cohort, the sensitivity will generally be much lower. A review of multiple studies on treadmill testing in elective and post-emergency room outpatient testing showed a consistent pattern.

A normal treadmill test does not imply that there is no underlying significant heart artery disease, with some studies reporting patients developing heart attacks within 30 days after a normal treadmill test. Stress testing generally detect arteries that are severely narrowed (70 per cent or more). Heart attacks can occur when the vessel lining separating the cholesterol deposits in the arterial wall is torn (plaque rupture) and triggers a biological cascade that results in the formation of a blood clot that occludes the arterial lumen.

Plaque rupture often occurs in less severe blockages. Generally, if you do not have major risk factors such as high cholesterol, diabetes mellitus, hypertension and/or smoking, the likelihood of underlying significant coronary artery disease is low if your treadmill test is normal.

If you have an abnormal treadmill test, it does not imply that you have significant heart artery blockage. For pre-menopausal women with no major risk factors for heart disease, there is a high likelihood that the abnormal treadmill test is a false positive test result. This can lead to further unnecessary testing.

For men with chest pain and/or shortness of breath on physical exertion, and have risk factors, an abnormal treadmill test indicates a high likelihood that there is underlying significant heart artery disease. Further evaluation will be deemed warranted in such a situation.

Evaluation after an abnormal treadmill test

While in the past, an invasive coronary angiogram – which involves inserting a plastic tube into your arteries under X-ray guidance – is often recommended after an abnormal treadmill test, there are more options today.

A study published in the New England Journal of Medicine in 2010 was conducted on almost 400,000 patients undergoing invasive coronary angiogram. It concluded that coronary angiography had a “low diagnostic yield”. Only just over a third of the patients in the study were found to have significant blockage of the heart arteries.

Invasive coronary angiograms carry a one-in-1000 risk of major stroke, heart attack or death. They also carry between 5 and 22 per cent risk of silent strokes, based on data from multiple magnetic resonance imaging (MRI) brain studies performed before and after the angiography.

Increasingly, alternative diagnostic methods have become available for those suspected to have coronary artery disease. These include functional tests such as nuclear myocardial perfusion scans, stress echocardiography, MRI myocardial perfusion scans , rubidium cardiac positron emission tomography (PET) scans, and anatomical scans such as computed tomography of the heart arteries (CT coronary angiogram) and MRI scans of the heart arteries.

Increasingly, CT coronary angiogram is being considered as one of the first-line options for the assessment of heart artery disease in many countries, including the United Kingdom, Europe and the United States. Unlike invasive coronary angiogram, CT coronary angiogram is an outpatient procedure that can be performed within seconds using newer generation of CT scanners after the injection of contrast media into the arm veins.

Given the multiple options available today, a discussion with your doctor will help you decide which is the most appropriate test after an abnormal treadmill test result.

When is sex too stressful for your heart?

WHILE having sex is a normal part of life, many wonder whether their heart can continue to withstand the excitement of sex when they grow older. Those with heart disease worry about the risk of precipitating a heart attack during sex.

Many with heart disease have associated risk factors such as diabetes mellitus, hypertension, smoking and medication, which may impair the ability to engage in sex. While the use of drugs such as Viagra may alleviate the situation, a common concern is the impact of such drugs on those with heart disease.

Sex as exercise

Sex does burn calories. With sexual arousal and physical exertion, adrenaline increases and the heart rate and blood-pressure increases. Most studies have shown that, despite the perception of sex being a vigorous physical activity, the heart rate generally remains below 130 beats a minute, and systolic blood pressure below 170, while having sex with a familiar partner.

On the average, middle-aged couples have sex about twice a week, each episode lasting about 15 minutes, and burning more than 50 to 80 calories depending on the intensity of sex.

Activities that will burn about 50 calories will include running up and down the stairs for three minutes or playing tennis for six minutes.

Will sex increase the risk of heart disease or stroke?

Though some people get headache during sex and worry about getting a stroke, a study published in the Journal of Epidemiology and Community Health found that frequency of sex was not associated with stroke in the 914 men they followed for 20 years.

A 10-year study on the sex habits of about 2,400 men in a town in Wales showed that those who reported the most frequent sexual activity were only half as likely to suffer a stroke or heart attack during that time. Hence, from an epidemiological perspective, sex does not increase the long-term risk of heart attack or stroke.

This could be partly explained by the reduction of stress and blood pressure with sexual activity. Studies reported in the journal Biological Psychology showed that cohabiting participants who had frequent sexual intercourse had better response to stress and lower diastolic blood pressure.

Sexual activity and orgasms increase the levels of the hormone oxytocin (also termed the “love hormone”).

Higher levels of oxytocin are associated with the urge to bond and with the feeling of generosity. As the level of oxytocin hormone increases, endorphins also increase. Endorphins have morphine-like effects on the brain and hence the sensation of pain declines. The oxytocin released during orgasm also promotes sleep.

Hence, you should not be surprised as to why your partner falls asleep so easily after sex. There is substantial data that getting adequate sleep is associated with a lower risk of heart disease and stroke.

Can sex cause a heart attack?

In a study published in the Journal of the American Medical Association, researchers from Tufts Medical Centre in Boston concluded that exercise and sex can increase the risk of heart attack and sudden cardiac death, although the increased risk is small and transient.

The risk is higher for those who exercise infrequently compared to those who exercise regularly. The researchers pooled together smaller studies that compared the risk of heart attacks and sudden death when participants were exposed to physical activity and engaged in sexual activity to times when they were not.

The study found that episodes of physical activity increased heart attack risk 3.5 times and risk of sudden cardiac death nearly five times.

Sexual activity increased heart attack risk 2.7 times but there was no data available on the link between sex and sudden cardiac death risk. The relative risk is a comparison of the risk when participants are exercising or having sex compared to the risk when they are not.

What it means is that physical exercise and sexual activity can trigger the onset of heart attack and sudden cardiac death, but that risk is transient and lasts for the one to two hours during and after the activity. While the relative risk of a heart attack during sex is 2.7 times, the absolute risk (that is, the probability of heart attack or sudden cardiac death actually occurring in an individual) is extremely small, at least during conventional sex with a familiar partner.

To look at it from another perspective, for a healthy 50-year-old man, the risk of having a heart attack in any given hour is about one in a million. Sexual activity doubles the risk, but even then, the risk is minuscule – just two in a million.

A study published in Lancet by Belgian researchers reported that 2.2 per cent of heart attacks is related to sexual activity. The million-dollar question for many men with heart disease is: “What is the risk of getting a heart attack during sex?” Yes, the risk is increased by 10 times compared to healthy men but even with this increased risk, the likelihood of getting a heart attack during sex is only one in 50,000.

A study on sudden cardiac arrest during sexual intercourse published in the Circulation journal in 2018 examined the data from the Paris-SDEC registry (Paris-Sudden Death Expertise Center). For those who had sudden cardiac arrest and were admitted alive to the hospital, less than one per cent were sex-related and occurred typically among middle-aged men with cardiovascular risk. About seven in 10 were due to underlying heart disease and about three in 10 were due to subarachnoid bleeding (bleeding between the skull and the brain), a type of intracranial bleeding due to rupture of an aneurysm of a brain artery.

ABCs of having sex safely

Most people with heart conditions want to know when they should avoid sex, and when they can begin having sex again. Avoid sex if you are unwell or if you detect symptoms of heart disease such as shortness of breath or chest tightness on exertion. If these symptoms occur during sex, stop immediately.

Not uncommonly, doctors are confronted with the question: “Is it safe for me to take Viagra?” Common drugs for males with erectile dysfunction (resulting in inability to complete sexual intercourse) include sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis). For those with heart disease, being able to exercise up to a heart rate of 130 per minute without any heart symptoms will generally indicate that it is safe to have sex, even with the use of such medication. There is one very important contra-indication – those who take nitrate medications cannot take these drugs.

Simply put, if you feel well after walking up the stairs for at least three floors, you can safely assume that your heart can withstand the “stress” of sex.

The highs and lows of blood pressure in older adults

BEYOND the wrinkles and the blemishes that come with advancing years, the invariable march of age will result in changes in the blood vessels that have served us so faithfully. Just as rubber becomes stiffer and less pliable over time, our arteries will also lose its elasticity and become less distensible. An effect of this is an increase in the upper or systolic blood pressure (SBP) value and labile fluctuation in SBP with varying levels of activities and emotional changes.

Hence, it is not uncommon to find in the elderly a blood pressure (BP) of 160/90 mm Hg at the doctor’s clinic, even though the preceding home BP recording showed 130/80 mm Hg.

“High” blood pressure that is normal

One elevated blood pressure reading does not mean that high blood pressure (hypertension) exists. While the pliable and elastic wall of the arteries in a young person allows the arteries to distend and “absorb” the increase pressure that is generated through an increase in heart rate or by stress, the loss in elasticity and stiffening of arteries with ageing means an elevation in the SBP will be more commonly seen with emotional stress, anxiety and physical exercise. Hence, in the elderly, the need to record blood pressure on multiple occasions at rest is necessary before a diagnosis of hypertension can be confirmed.

However, office and home blood pressure measurements may still be elevated in the situation of “pseudo-hypertension”, a condition where the SBP is falsely elevated because of significant stiffening and hardening of the walls of the arteries. In this situation, the cuff inflation during blood pressure recording may have to be inflated to very high pressures before the artery can be compressed, resulting in a highly elevated SBP value and a normal lower or diastolic blood pressure (DBP) value.

This may be more often seen in those who have diabetes mellitus where diffuse hardening of the arterial wall is more commonly seen. Furthermore, smaller arteries are more likely to be affected as compared to larger arteries.

Hence, in this situation, it may be better to use an arm BP measuring device rather than a wrist BP measuring device. This condition should be suspected if there are absolutely no symptoms and no evidence of any damage to any organs, despite the BP being persistently high and not responding to medication.

The three situations of labile SBP elevation, “white-coat hypertension” and “pseudo-hypertension” are more prevalent in the elderly and a correct diagnosis is important in avoiding overtreatment.

Impact of high blood pressure

Persistent elevation of high BP can manifest itself by the presence of damage to the brain (stroke, bleeding, dementia), the heart (chamber enlargement, abnormal heart rhythms), major blood vessels (aneurysm or enlargement of the aorta), kidneys (impairment of function) and eyes (degeneration of eyesight).

An objective way to assess the effect of persistent hypertension is to evaluate the impact of high BP on the heart. The left-side heart chambers are connected to the aorta, the main arterial channel which supplies blood to the entire body. In persistent poorly controlled hypertension, the thinned walled left upper heart chamber will be enlarged and the muscular left lower chamber will have thickened walls as the heart chamber has to pump harder against a higher BP for the blood to enter the aorta. This can be objectively confirmed by an ultrasound examination of the heart, which is also called echocardiography.

The absence of these changes on echocardiography in the presence of persistently high BP not responsive to medication and yet not accompanied by symptoms should lead one to suspect “pseudo-hypertension”.

How low should the blood pressure be?

The latest American College of Cardiology and the American Heart Association guidelines recommend that older adults with a BP of 130/80 mm Hg or higher should be treated. Under normal resting conditions, about 85 per cent of the blood perfusion of the muscle of the main heart pumping chamber, the left ventricle, occurs during diastole (relaxation phase of the heart chamber). Hence, the arterial diastolic BP (DBP) is the main force that “pushes” blood into the heart arteries to perfuse the left ventricle muscle.

Presently, we do not know what is the lowest limit of DBP where it is not able to maintain adequate perfusion to the left ventricle muscle. In patients with heart artery disease, if the cross-sectional area of the heart artery is reduced by more than 70 per cent , there will usually still be adequate perfusion due to compensatory dilatation of the microcirculation but the maximum heart artery blood flow will be reduced.

If the cross-sectional area reduction is at least 85 per cent to 90 per cent, there can be inadequate perfusion even at rest. Hence, in those with significant blockage of the heart arteries, the DBP should not be excessively low and should be individually titrated. Likewise, in those with significant narrowing of the brain arteries, a sudden drop in the SBP can precipitate a stroke. Hence, for the elderly diabetics who are at a higher risk of developing heart and brain artery disease, caution should be exercised.

In the ACCORD BP trial that looked at intensive BP lowering in diabetics, intensive BP control (SBP <120 mmHg) did not reduce the combined major cardiovascular complications (heart attack, stroke and death). However, when the outcomes were looked at individually, there was a reduction in stroke at the expense of increased serious adverse events. Hence, while achieving BP targets <140/90 mmHg may be suitable for some diabetics, not all will be better off with intensive BP lowering (SBP <120 mmHg).

In the International Database on Home Blood Pressure in Relation to Cardiovascular Outcome (IDHOCO) study published in Circulation journal in 2015, for those hypertensive octogenarians treated, a SBP of less than 127 mm Hg was associated with increased death and the lowest risk was at a systolic BP of about 149 mm Hg. Hence, for hypertensive octogenarians, as a result of age-related decreased circulation to the organs and a higher risk of a postural drop in BP on standing, maintaining the SBP between 150 mmHg and 140 mmHg is the sweet spot.

Should I worry about the pain in my chest?

Should you worry about the chest discomfort you have been having lately? Every so often, when you are jogging, playing your game of tennis or while you are enjoying your game of golf, you may have felt that discomfort in the chest and wondered whether to dismiss it or take it as a warning of underlying heart disease. This is a common dilemma.

Worrisome chest discomfort

Chest discomfort or pain is the most common complaint encountered by family physicians, cardiologists, and emergency-room physicians. What distinguishes the chest pain due to underlying blockage of the heart arteries (angina pectoris) from other types of chest pain are the characteristics of the pain. The term angina pectoris is derived from the Latin word angina (“infection of the throat”), the Greek ankhone (“strangling”), and the Latin pectus (“chest”), and can therefore be translated as “a strangling feeling in the chest”.

Hence, during exercise, the increased demand for oxygen is met primarily through increased blood flow through the heart arteries. If there is an obstruction to blood flow because of the narrowing of heart arteries, the oxygen supply may be unable to meet the increased demand, resulting in an environment where there is insufficient oxygen. This results in the activation of cellular pathways which operate in an oxygen-scarce environment, resulting in the production of chemicals such as lactic acid. The build-up of these chemicals stimulates nerve endings that cause the sensation of pain.

Angina or heartburn?

Heartburn is an uncomfortable feeling of burning or warmth in the central chest, which may radiate to the neck, throat, and jaw. It can mimic angina and present itself as chest tightness. Unlike angina, it is not due to heart disease, but is a result of backflow of acid from the stomach into the oesophagus (gastroesophageal reflux disease or GERD). It is typically aggravated by lying down or bending over soon after a meal and relieved by standing up, drinking water, and taking antacids. It is present in about one-third of adults, especially in pregnant women. It can sometimes be difficult to distinguish it from angina, the main distinguishing factor being that heartburn is not related to exertion.

Angina in the young

If you are young and have chest tightness or shortness of breath while running and never seem to be able to keep up with others during exercise, it may not be that you are not physically fit. There is also a possibility that you may have underlying congenital heart artery disease. Angina can occur in the young as a result of inherited conditions. For the majority, while the major heart arteries lie on the surface of the heart, in some, the artery may take a course where a segment of the artery may be embedded in the heart muscle (myocardial bridging) and hence the embedded segment may be compressed by the heart muscle bands during contraction of the heart.

If a long segment is embedded deeply into the heart muscle, the obstruction to flow may be significant enough to cause angina during vigorous physical exertion. Another rare cause of mechanical obstruction is the abnormal origin and course of the heart artery, where a segment of it is wedged between the main artery arising from the heart (aorta) and the lung artery (pulmonary artery). During heavy physical exertion, the pulsations of the two large arteries may result in compression of the heart artery to the extent that it causes angina. On rare occasions, these two inherited causes of heart artery obstruction can cause sudden death during vigorous physical exertion in the young.

Angina not related to exertion

While angina is typically associated with physical exertion, there is an uncommon variety called coronary vasospasm or Prinzmetal’s angina. This condition is due to transient constriction of the heart artery secondary to abnormalities in the regulation of the smooth muscle in the wall of the artery. The angina associated with spontaneous spasm of the heart artery usually develops during sleep or early in the morning. In some patients, chest pain development is associated with alcohol drinking and one interesting feature is that the chest pain episode tends to develop several hours after alcohol intake, rather than occurring immediately after drinking. Hence, these patients may be mistakenly diagnosed to have gastrointestinal problems including stomach ulcer disease or GERD. Coronary vasospasm, if unrecognised, can result in heart attacks and sudden cardiac death.

Chest pain but not angina

Understanding angina will help to distinguish the types of chest pain that do not need urgent medical attention. Chest pain is usually not angina if it can be localised to a single site on the chest using two fingers, is sharp, pulling or pinprick in nature, and not aggravated by exertion. If you are young and cannot seem to be able keep up with your friends when running, the presence of chest pain during running may suggest that you may have an underlying inherited heart artery condition. Medical advice should be sought before embarking on vigorous endurance exercise activities such as marathons. If you have multiple risk factors for heart disease and have typical exertional anginal chest pain, it is very likely that you have underlying blockage of your heart arteries. You should have your heart assessed by your doctor before attempting vigorous physical activities.

However, if you have risk factors for heart disease and have no symptoms, do remember that having no chest pain does not mean there is no heart disease. In a US study on out-of-hospital sudden cardiac arrest published in the Circulation journal in 2006, only about 25 per cent had angina prior to the sudden collapse. In that study, only 6 per cent survived the sudden cardiac arrest and were discharged from the hospital alive. Hence, controlling your risk factors and having regular follow-up with your doctor is the best way to prevent sudden death.

Life extension – health, rejuvenation and longevity

The relentless pursuit of the elixir of youth has spurred anti-ageing research in attempts to achieve the triple goals of life extension, namely, the triumvirate of healthy lifespan, rejuvenation and longevity. Sirtuins are a family of cellular enzymes that are powered by a chemical compound called nicotinamide adenine dinucleotide (NAD). They play an important role in preventing diseases and even reversing some aspects of ageing. Studies have shown that increased sirtuin activity in mammals has been associated with a delayed onset of age related diseases and increased longevity.

Increased sirtuin activity appears to inhibit nerve degeneration and reduces the development of cardiovascular and metabolic diseases (such as diabetes mellitus and abnormal lipid levels). Hence, if sirtuin activity can be increased using compounds that can boost its activity (STACs or Sirtuin Activating Compounds), the use of STACs can potentially help a person stay healthy longer, even if longevity is not affected.

Resveratrol
Resveratrol is a natural plant phenol STAC found in the skin of red grapes and other fruits such as blueberries and cranberries. Contrary to common belief, red wine contains very little of it. Resveratrol has been shown to have life-extending properties in studies on lower-order species such as yeast and nematodes, but this effect has marginal reliability in higher-order species. Nevertheless, it has been shown to have potentially beneficial effects. Before you start taking large doses of resveratrol, you may be surprised to know that it is a Janus-faced compound.

Low dietary doses may suffice to elicit the biological responses required to optimise the body’s defence mechanisms against incipient disease. But at high doses, it behaves in a contrarian manner. At low doses, resveratrol induces responses that overlap with the female hormone oestradiol. Low-dose effects seen in animal and human studies include beneficial metabolic effects such as more efficient glucose reduction in diabetics, reducing the development of obesity and non-alcoholic fatty liver disease, protecting against arterial degeneration, delaying development of neurodegeneration, and improving motor and cognitive functions.

At high doses, resveratrol has an anti-oestrogen effect which suggests that it may reduce the risk of oestrogen- dependent cancers. This Janusfaced hormetic effects of resveratrol may partly explain the French paradox, where there is a reduced incidence of cardiovascular diseases and certain types of cancer in some populations despite their consumption of high-fat diets.

NAD
NAD is an important molecule that is essential for over 500 enzyme reactions in the body which impact metabolism, ageing, cell death, DNA repair, and gene expression. Hence, NAD plays a pivotal role in human health span and longevity and is a necessary substrate for sirtuin enzymatic activity. In mammalian cells, NAD is mainly generated by the conversion of nicotinamide (a soluble form of Vitamin B3) into nicotinamide mononucleotide (NMN) followed by its combination with another molecule to form NAD. There is also another precursor, nicotinamide riboside (NR), that is converted by enzymes to NMN in the cells. As this pathway is safe and also the most efficient route for production of NAD, NMN or NR supplementation has been used to increase NAD levels.

Animal studies have shown that NMN supplementation can ameliorate the age-related reduction in NAD production in cells and improve the body’s cardiovascular response to ageing. Age-related decrease in arterial elasticity means that the aorta is less able to expand and buffer the increased blood pressure generated each time the heart pumps. With ageing, the production of a pressure-bearing protein, type 1 collagen, in the arterial wall increases, whereas the main protein responsible for the structural integrity and elastic properties of the arterial wall, elastin, decreases. Studies in mice have shown that NMN supplementation was able to reduce stiffness in large arteries by reversing the accumulation of type 1 collagen in arterial walls and improving elastin content.

From the age of 40 years onwards, there is a gradual decline in perfusion of the body tissues resulting in gradual deterioration in body function towards the last decades of life. A consequence of this is cognitive decline. Optimal brain function is dependent on adequate oxygen and nutrient delivery via minute brain blood vessels (cerebral microvascular circulation). This modulation of brain blood flow in response to increased brain activity is impaired with age, contributing to age related cognitive impairment. Studies in aged mice given NMN have demonstrated an improvement in the modulation of cerebral microvascular circulation. Animal studies have also shown that NMN can prevent age-related cognitive decline by reducing cell death in areas of the brain that control short and long-term memory.

Use of NMN was also associated with decrease in the neurodegenerative changes seen in Alzheimer’s disease and age-related retinal changes. This age-related decrease in the production of new vessels and a gradual decrease of blood vessels in the microcirculation also result in reduction in muscle mass and diminishing exercise capacity with age. Mice given NMN were able to demonstrate an increase in the production of new vessels in the muscle and an increase in density of small vessels, thereby improving exercise capacity.

Caloric restriction
Caloric restriction (CR) which involves calorie reduction without causing malnutrition, has been associated with an increase in lifespan in some animal studies. In these studies, dietary CR was associated with increased lifespan and reduced disease incidence,  specially cancers. However, some studies did not show benefit and, in some mouse strains, CR was associated with shortened lifespan. Observational studies on humans who have practised extreme CR over many years showed low levels of risk factors for cardiovascular disease and diabetes. Similarly, a human study on CR, the CALERIE study, found that CR participants had lower blood pressure and lower cholesterol. The study was too short to examine the impact of CR on lifespan. The current conclusion from the National Institute of Aging in the United States is that there is not enough evidence to recommend CR as a therapeutic measure for life extension.

Although CR was associated with lower risk factors for cardiovascular diseases and diabetes, caution is urged as in a study using mouse lemurs on prolonged CR, MRI studies showed that there was more widespread age-related grey matter atrophy in CR animals while only a few regions in the brain showed atrophy in those not on CR.

Life extension
Globally, heart disease and stroke are the two main causes of death in most high-middle and high-income countries. Hence, the first cardinal principle in life extension is to control the risk factors such as blood pressure elevation, cholesterol elevation, sugar elevation and smoking. The second principle is to have a healthy lifestyle such as keeping the weight within the healthy range and exercising regularly. Both physical exercise and dietary CR result in a significant increase in NAD production and increase sirtuin activity. CR may be an option as part of a weight-reduction regime to keep the weight optimal. The third principle is to see your doctor regularly to control risk factors.

Finally, among the supplement options, scientific studies favour the use of low-dose resveratrol or NMN as they may potentially provide many health benefits via increased sirtuin activity, although more studies will be required to understand their efficacy in human life extension.

Unravelling the holy grail of anti-ageing and longevity

GOOD nutrition, clean environments, accessibility to good healthcare and healthy lifestyles have increased human longevity. Nevertheless, the quest of increasing longevity is insatiable. As medical science pushes the boundaries of human lifespan, delving into the science of longevity can help us sieve through the reams of information and distil the essence of anti-ageing and cell preservation.

Cellular ageing

Cell ageing or cellular senescence is a physiological state with permanent cessation of the ability of the cell to replicate and accumulation of damaged DNA ( basic building blocks of genes), and this process is increased by ageing. This cellular senescence is marked by shortening of the protective terminal ends of the chromosomes which are called telomeres. Telomeres are like plastic caps at the ends of shoelaces, preventing them from being frayed and damaged. Shortening of the telomere is a sign of cellular senescence. In 1979, the first of the SIR (silent information regulator) proteins or sirtuins was reported. Over time more members of this protein group were found. In 1999, the publication of a study that reported that increased sirtuin activity could increase the lifespan of yeast cells by 70 per cent heralded a major breakthrough that accelerated the interest and research in sirtuins. Since then, there has been a growing body of evidence that the cell has a group of anti-ageing proteins, the sirtuins, that are essential for delaying cellular senescence and increasing the lifespan of organisms.

Anti-ageing proteins

Core to the science of anti-ageing is this group of proteins called sirtuins. In human cells, there are seven sirtuins (SIRT 1 to 7) with various roles within the cell. Three of these sirtuins (SIRT 3,4,5) control the generation of power for the needs of the cells and function in the mitochondria (power generator which produce the energy for the needs of the cell) with roles in cellular antioxidant balance and lipid metabolism. Another three sirtuins (SIRT 1, 6, 7) control the genetic framework in the cell and function in the cell nucleus (the central core of the genetic material in the cell) with roles in gene expression and DNA repair. There is one sirtuin (SIRT 2 mainly) which control the environmental processes within the cell and function in the cytoplasm (the liquid content within the cell). As an analogy, if the cell is a factory, the sirtuins are the executive management of the company directing and controlling all the aspects of the cell’s activities. They play important roles in maintaining the integrity of the cellular genetic structure, keeping the genetic material (chromatin) in a “wound up” protected state to reduce damage and in repairing damaged DNA.

Mechanisms of action

The main mechanisms of suppression of cellular senescence by sirtuin activity is via the actions of preventing telomere shortening or attrition, and promoting the repair of damaged DNA. Many proteins in the cells have a chemical tag called an acetyl group attached to it. One of the key ways in which sirtuins work is by the removal of the acetyl group from other molecules or proteins, thereby affecting the activity of the protein. This action has significant impact on the control centre of the cell, namely the activity of the genetic material or chromatin.

The basic building block of the genetic material, the DNA, is wrapped around groups of proteins called histones allowing the genetic material (chromatin) to be packed more compactly. When the histone protein has the acetyl group chemical tag , it causes the chromatin to be partially unwound and hence exposing the unwound DNA to be copied, thereby allowing the gene instruction to be passed to another cell or protein. As an analogy, it is as if a door to the office is opened and people are allowed to go into the office to copy instructions which are then passed to other offices. Once all the instructions are copied, the office door is closed. Hence, once the task is completed, the chromatin will not remain unwound as it will be more vulnerable to damage if it remains open.

Subsequently, the sirtuins can then remove the acetyl group from the histones which will then allow the chromatin to be closed by being “wound up” tightly, preventing DNA material from being copied and in effect silence the gene. Besides histones, sirtuins target other non-histone proteins such as proteins involved in copying genetic information and proteins that are involved in the repair of DNA. They are also known to regulate the production of the enzyme telomerase which is required for telomere elongation and maintenance of the integrity of the telomere. Most human cells have insufficient telomerase and hence there is progressive shortening of the telomere which is strongly indicative of progressive cellular ageing. Elongation of the chromosomal telomere is tantamount to reversing the biological clock.

Beneficial effects of sirtuin activity

Studies have shown that sirtuins have roles in the regulation of copying of gene information, modulation of energy production, prolongation of cell survival, reduction of DNA damage, reduction of cell damage and prolongation of longevity. Increased sirtuin activity in mammals has been associated with a delayed onset of age-related diseases and an increase in longevity. Sirtuins appear to be able to inhibit axonal (nerve fibre) degeneration, a process that often precedes the death of nerve cells as seen in neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease.

It may also have protective effect on nerve cells, reducing processes that lead to the death o f nerve cells and the development of Alzheimer’s disease. Loss of sirtuin activity has been implicated in the development of cardiovascular and metabolic diseases including degeneration of arteries, acute damage to the heart muscle, thickening of the heart muscle, abnormal heart rhythms, high blood pressure, obesity, diabetes mellitus and abnormal lipid levels. While most of the studies have been done in animals, there is an increasing number of human studies.

There is presently an increasing body of evidence that shows increased sirtuin activity is indispensable for delaying cellular senescence and appears to protect the body against many age related diseases. In addition, studies support the role of sirtuins as anti-aging agents and potentially prolong longevity. Hence, lifestyle, dietary and pharmacological choices that increase sirtuin activity can potentially increase the anti-ageing effects and prolong longevity. These will be discussed in the next article where we will examine how we can make better decisions to increase our quality of life and lifespan.

A Checklist Before Exercising To Prevent Sudden Cardiac Death

If you are deciding on starting an exercise programme to get yourself fit and healthy, you should tick off some boxes to ensure that you reduce your risk of sudden cardiac death (SCD). SCD is sudden unexpected death caused by the onset of a life-threatening heart rhythm (sudden cardiac arrest). In Singapore, it is estimated that about 1,000 individuals die of SCD every year. A 2017 Singapore study on SCD reported that the median age of SCD victims was about 47 years in males and more than 50 years for women. The largest cause of natural death in many developed countries including the USA is sudden cardiac death (SCD). SCD accounts for about half of heart-related deaths in the USA. It is also the most frequent medical cause of sudden death in athletes.

In SCD, there is a malfunction of the electrical system in the heart and the heart rhythm suddenly becomes very fast and irregular. This life-threatening heart rhythm (ventricular fibrillation or VF) will cause the pumping chambers (ventricles) of the heart to “quiver” instead of pumping blood to the body. This will result in a large drop in blood pressure, severe reduction of blood flow to the brain, loss of consciousness and death if no emergency measures are instituted. In the USA, if sudden cardiac arrest occurs outside a hospital, the one-year survival rate after hospital discharge is only about 10 per cent.

Heart attack does not equal sudden cardiac death In coronary artery disease (CAD), the coronary or heart artery is gradually narrowed and when the artery suddenly gets completely blocked (usually by a blood clot), a heart attack occurs resulting in damage to the heart muscle. This may result in instability of the heart rhythm and the development of VF. If VF occurs, and emergency measures are not instituted immediately, SCD ensues. However, not all heart attacks result in life-threatening heart rhythms. Hence, SCD can occur in seemingly “normal” individuals without any symptoms or warning in the absence of heart attacks. Causes of sudden cardiac death Coronary artery disease (CAD) is the most common cause of SCD and accounts for about 80 per cent of all SCD.

What is interesting is that in a recent Australian study on SCD in the young (published in October 2020 in the Circulation: Cardiovascular Quality and Outcomes journal) the most common cause of SCD in those 35 years or younger was CAD. accounting for 40 per cent of SCD. If this is further segmented into different age groups, CAD accounted for 50 per cent of SCD in those aged 26 years to 35 years. In those 5 years and below, inflammation of the heart muscle (myocarditis) was the main cause of SCD and in those 6 to 15 years, myocarditis accounted for 25 per cent of SCD. Other than CAD and myocarditis, the other two main underlying causes of SCD were:
* those who die from an electrical malfunction (arrhythmia) with a structurally normal heart but no other cause found (otherwise known as sudden arrhythmic death syndrome or SADS)
* those with a structurally abnormal heart (swollen heart such as dilated cardiomyopathy or abnormal thickening of the heart muscle such as hypertrophic cardiomyopathy).

Less common causes of SCD include tear of the aorta (aortic dissection), heart valve disease and congenital heart disease. Sudden cardiac death in athletes The SCD profile is different in competitive athletes with most SCDs occurring during intense exertion, and the  common causes of SCD being SADS, heart muscle disease and coronary anomaly (abnormal heart artery). In one study, it was reported that in competitive athletes, SCD was due to SADS in 42 per cent of the cases followed by heart muscle disease (40 per cent). An American College of Cardiology article in December 2019 stated that recent data from the National Collegiate Athletic Association suggested that the most common finding at autopsy for SCD cases was a structurally normal heart (25 per cent), implying that abnormal heart rhythm is likely to be the most common cause of SCD. The second commonest cause was coronary anomaly followed by hypertrophic cardiomyopathy.

This is different from Italian studies, where the most common cause of SCD in athletes was arrhythmogenic right ventricular cardiomyopathy (ARVC), which accounted for about 25 per cent. ARVC is a genetically inherited heart muscle disease where the right ventricle muscle wall has been replaced with abnormal scar tissue causing electrical instability and an increased disposition to VF. The risk of VF is increased by exercise. Generally, in athletes, the data is consistent that electrical malfunction of the heart, heart muscle disease and abnormal heart artery are the three commonest causes of SCD, unlike the general population where CAD is the commonest cause of SCD. Checklist to reduce risk of sudden cardiac death As the consequences of SCD are often devastating, preventing SCD is a key priority.

This means that we need to identify those at risk of SCD. As CAD is the main cause of SCD even for the young , identifying those at risk of CAD is one of the best ways to prevent SCD. Check out this pre-exercise risk identifier list before you embark on vigorous exercise:
* Do you have risk factors for CAD such as high cholesterol, smoking, hypertension, diabetes mellitus, or family history of heart disease?
* Did you have significant damage to your heart because of a previous heart attack or did you have a heart attack within the last 6 months?
* Did you have a previous episode of sudden cardiac arrest?
* Do you have a family history of sudden cardiac arrest or SCD?
* Do you have pre-existing abnormal heart rhythms?
* Do you have unexplained fainting episodes?
* Do you have exertional chest tightness or shortness of breath?
* Are you on medication that can potentially increase your risk of abnormal heart rhythm such as diuretics (can cause abnormally low blood potassium or magnesium levels) or rhythm controlling drugs?
* Do you have a history of congenital heart disease?

If your answer is yes to any of the questions above, you should seek your doctor’s advice before embarking on your exercise programme.

Pre-exercise screening
Both the American Heart Association and the European Society of Cardiology (ESC) advocate pre-participation screening (PPS) of young athletes as intense athletic activity can trigger SCD or disease progression in susceptible individuals. While both recommend a thorough medical and physical examination, only the ESC recommends a routine 12-lead electrocardiogram (ECG) to detect underlying electrical abnormalities or heart muscle disease. However, it is important to understand the limitations of the ECG. For example, the ECG is normal in most individuals with congenital coronary anomalies, in 5 to 10 per cent of those with hypertrophic cardiomyopathy, and in most individuals with catecholaminergic polymorphic ventricular tachycardia (life-threatening heart rhythm).

Those athletes with abnormal findings during the PPS will require further assessment. In addition, the American Heart Association recommends that for men who are 40 years and older and women who are 50 years and older, an exercise stress test may also be required depending on the assessment by their doctor. If heart problems are identified or suspected during the screening, the individual should be referred to a heart specialist for further evaluation before embarking on an exercise programme. As CAD accounts for about 80 per cent of SCD, it means that ticking off the boxes before embarking on exercise and getting appropriate medical advice can prevent SCD in most high-risk individuals.

Should cholesterol lowering medication be started in the young?

Earlier treatment of elevated cholesterol results, even for children when indicated, results in better outcomes

While the general perception is that strokes only occur in the elderly, over the years, there has been a gradual increase in the prevalence of strokes in the young. Recently, a young patient of mine, who is in his 20s with multiple risk factors for heart disease and stroke, was found to have near complete occlusion of one of his major arteries in the brain, the middle cerebral artery (MCA). The MCA provides blood supply to the part of the brain that controls power, sensation and speech. A stroke involving this artery will not only result in severe disability but can also be life threatening.

Stroke in the young

Severe narrowing of an artery within the skull is termed as intracranial stenosis and encompasses narrowing of the brain arteries. Intracranial stenosis is a common cause of stroke and is particularly prevalent in Asians. In a 2017 study on young Chinese with intracranial stenosis published in the Annals of Translational Research, it was found that in about 80 per cent of those with unilateral blockage of the MCA, the underlying cause was attributable to atherosclerosis. Atherosclerosis is the condition where there is narrowing of the arterial wall (plaque formation) due to the build-up of fat, cholesterol, calcium, and other substances found in the arterial wall. While atherosclerosis remains the main cause of blockage of brain arteries in the young, there are also other causes such as vessel malformation (Moyamoya disease), inflammation of vessels (vasculitis), abnormal arterial wall growth (fibromuscular dysplasia), tear of the artery (arterial dissection); however, these are more prevalent in young females.

Earlier studies showed that for those with significant intracranial stenosis, there was about a one-in-eight chance of getting a stroke or even death within a one- to two-year period even with medical treatment. A more recent publication on the Oxford Vascular Study in May 2020 in Lancet Neurology demonstrated that the risk of intracranial stenosis stroke for those on intensive medical therapy was lower when compared to previous studies, being 5.6 per cent one-year risk (compared to 9.4 per cent in VISSIT, a study on treatment of intracranial stenosis) and 5.6 per cent two-year risk (compared to 14.1 per cent in SAMMPRIS, a study on treatment of intracranial stenosis). The better outcomes in the Oxford Vascular Study may be explained by better medical treatment available in more recent years. In the Chinese Intracranial Atherosclerosis (CICAS) Study, the highest rate of recurrent stroke was seen in those with three or more risk factors.

The major risk factors include high cholesterol level, diabetes mellitus, smoking and high blood pressure. Hence, optimal control of risk factors is essential in those with intracranial stenosis.

Atherosclerosis in children and young adults

While it may come as a surprise to many that the young can develop significant blockage of arteries, the data proving that atherosclerosis is prevalent in the young has been around for some time. Autopsy data from young men with a mean age of 22 years who died during the Korean war showed that more than 70 per cent of them had atherosclerosis in their heart arteries. A similar study on young Americans who perished in the Vietnam war showed that 45 per cent had atherosclerosis and 5 per cent had severe heart artery atherosclerosis. Studies on younger cohorts showed evidence of early onset atherosclerosis in children. A study of young American motor accident victims showed that more than 50 per cent of children aged 10 to 14 years have evidence of early atherosclerosis. In the Bogalusa Heart Study, early atherosclerosis (presence of fatty streaks in the heart arteries) was present in about 50 per cent of those aged from two to 15 years.

Never too young for prevention

Cholesterol remains the single most important risk factor for stroke and heart disease. While it is almost unthinkable in the past to consider starting children on cholesterol-lowering drugs (statins), there is now almost universal agreement that in those with familial hypercholesterolaemia (genetically high cholesterol levels), treatment should commence at a young age. The European Atherosclerosis Society (EAS) consensus panel and the latest American College of Cardiology-American Heart Association (ACC-AHA) guidelines for familial hypercholesterolemia recommend that statins be commenced from as young as eight years (EAS) to 10 years (ACC-AHA) of age. In October 2019, the New England Journal of Medicine published a 20-year follow-up study of children with familial hypercholesterolemia who were started on statin medication at an age of eight to 18 years.

Their results were compared with their affected parents with familial hypercholesterolemia who were only given statins much later in their lives. At the end of the follow-up period, 99 per cent of young patients receiving statins had cardiovascular disease-free survival compared to 74 per cent for their affected parents. This meant that earlier commencement of statin therapy in these at-risk young patients resulted in better long-term outcomes. The latest consensus from the EAS and the International Society of Atherosclerosis (ISA) is that it is not a hypothesis but a fact that LDL cholesterol (“bad” cholesterol) is a major determinant of atherosclerosis. The development of atherosclerosis in arteries is not just dependent on the absolute LDL cholesterol level but also by the cumulative exposure of the arterial wall to LDL cholesterol.

Hence, preventing the development of atherosclerosis not only embodies the concept of “the lower the better” with respect to the LDL cholesterol level, but also a newer concept that “the younger the better”, meaning earlier treatment of elevated cholesterol results in better outcomes.

Early detection

While prevention remains the cornerstone of management, there will be invariably some at-risk young people who may get a stroke. Understanding the symptoms is a key step in early detection and management. Patients with significant intracranial stenosis can present with symptoms of a transient insufficiency in blood flow to the brain (transient ischemic attack) or a stroke. While symptoms such as weakness of one side of the body, slurring of speech, and numbness of one side of the body are easily recognised as an evolving stroke, other symptoms such as severe headache, changes in vision and severe dizziness or a spinning sensation (vertigo) are less well recognised as symptoms of stroke. While ultrasound of the neck (carotid) arteries is commonly used to assess the risk of stroke, it has its limitations. In the CICAS Study, only 20 per cent of those with intracranial stenosis had co-existing neck carotid artery disease, which means that the absence of disease in the neck carotid arteries does not mean that there is no significant intracranial stenosis.

For patients with symptoms, an MRI of the brain and brain arteries can provide confirmation. In an acute stroke, a CT scan of the neck and brain arteries is usually performed at the Emergency Department to help the doctor make a decision on therapeutic choices. In summary, evolving lifestyle and dietary changes have resulted in the development of atherosclerosis in children and young adults. Elevated LDL cholesterol remains the key driver of atherosclerosis and early management, even for children when indicated, can lead to better cardiovascular disease-free outcomes.

10 ways to lower your blood pressure without medication

Making changes to your lifestyle will help give you a healthy head start in life

Can you lower your blood pressure without taking medication? The answer is yes. If you have abnormally elevated blood pressure (BP) or hypertension, you may want to consider non-pharmacological measures initially rather than commencing on drug therapy immediately. Here are 10 ways to lower your BP without taking medication.

  1. Exercise

It has been shown that after a single session of moderate intensity aerobic exercise of a duration of 10 minutes or more, the BP can be reduced by 5 to 7 mmHg in people with high blood pressure. The good news is that this BP reduction can be sustained for up to 24 hours after the exercise session. This BP reduction is termed as post-exercise hypotension or PEH. The exercise should preferably be 30 minutes a day or a total of 150 minutes or more of exercise per week. Evidence shows that PEH benefits occur more with aerobic exercises such as walking, jogging, cycling or swimming as compared to dynamic resistance training using weights or resistance machines. In terms of exercise intensity, it should be at least be the equivalent of brisk walking which would increase your heart rate and breathing but does not make you feel out of breath.

  1. Cut salt intake

There is strong evidence that reduction of salt or sodium intake will result in a reduction of blood pressure. For those with high BP, they should not take more than 2,400 mg of salt per day which is equivalent to about 1 teaspoon of table salt. If the salt intake can be further reduced to 1,500 mg per day, there can be as much as 7 mmHg reduction in the systolic blood pressure and 3 mmHg in the diastolic blood pressure. The reduction in salt intake not only decreases the blood pressure but it is also associated with reduction in cardiovascular morbidity and mortality.

  1. Weight reduction

Studies in diverse populations have consistently shown a nearly linear relationship between body mass index and systolic and diastolic BP. Data from the long term US Framingham Heart Study estimated that about three-quarters of high BP in men and two-thirds of high BP in women can be ascribed to excess weight gain. The increased fat accumulation in the abdomen in obese individuals can result in an increase in the pressure within the abdomen to as high as 40 mm Hg. This not only results in compression on the kidney but also increases the pressure within the kidney and the kidney vessels. These changes have been associated with the development of high blood pressure and chronic kidney disease. It has been shown that keeping your BMI below 25 kg/m2 is effective in preventing the development of high blood pressure. It is estimated that a weight reduction of about 10 kg can potentially reduce the systolic blood pressure by 5 to 20 mmHg.

  1. Stop smoking

There is some controversy about the impact of smoking in blood pressure. Nevertheless, it is known that smoking causes various adverse cardiovascular problems and acts synergistically with high blood pressure to increase the risk of heart artery disease, heart attacks, sudden cardiac death, and stroke. Hence, for those with hypertension, smoking cessation is advocated.

  1. Treat obstructive sleep apnoea

In recent years it has been shown that obstruction of the upper airway during sleep, a condition termed as obstructive sleep apnoea or OSA, may actually contribute to elevation in BP, poor control of hypertension and even hypertension that is resistant to drug therapy. OSA leads to poor sleep quality and a sleep duration of less than or equal to five hours per night has been shown to significantly increase risk for hypertension in patients 60 years of age or younger. Treatment of OSA may improve the blood pressure control.

  1. Eat potassium-rich foods

It has been shown that potassium can decrease both the systolic and diastolic BP possibly by causing the body to remove more salt in the urine and by relaxing the walls of the blood vessels. However excessive potassium supplements can be harmful and is generally not encouraged by doctors. Hence, instead of taking potassium supplements, the American Heart Association advises that eating potassium rich foods may help to manage the blood pressure. These foods may include dried apricots, spinach, tomatoes, avocados, mushrooms, prunes or a fat-free yoghurt or milk.

  1. Eat magnesium-rich foods

Review of trials on magnesium supplementation concluded that consumption of 300 mg of magnesium a day can cause a modest reduction of diastolic BP but has no significant impact on the systolic BP. However, excessive consumption of magnesium from supplements may cause diarrhoea. There are currently no known adverse effects of magnesium intake from food. It is best to get magnesium from foods that include dark leafy green vegetables, nuts, unrefined grains and legumes.

  1. Consume cocoa

An analysis of more than 30 studies on cocoa have shown that consumption of cocoa was associated with about 2 mm Hg lowering of both systolic and diastolic BP. Hence the consumption of dark chocolate or cocoa products can be beneficial and this benefit is mediated through chemical compounds in the cocoa products called flavanols and it is believed that the blood pressure lowering of these chemicals are related to their ability to widen the blood vessels through a chemical called nitrate oxide.

  1. Take folate supplement

Studies have shown that the intake of folate, which is a type of Vitamin B, among patients with high blood pressure or hypertension may reduce the risk of stroke and aid in stroke prevention in patients with hypertension. Hence, for those with high blood pressure, consumption of folic acid may help to reduce the risk of stroke.

  1. Reduce stress

While researchers are not certain about the relationship between stress and the development of hypertension, they are clear that stress can cause significant transient elevation of blood pressure. It is possible that long-term stress can result in frequent, temporary spikes in blood pressure that can damage the blood vessels, heart and kidneys. Stress management includes getting sufficient sleep, adopting relaxation techniques such as meditation or yoga, widening your social circle by participating in support groups or classes, improving on time management, resolving stressful situations amicably, caring for yourself by doing the things you enjoy and asking for help when you need it.

These 10 ways to lower your blood pressure can make a difference to your life. Research has shown that a reduction in systolic blood pressure of 5 mmHg can reduce death from stroke by about 14 per cent, death from heart disease by 9 per cent and death from all causes by 7 per cent. Recent data show that lowering blood pressure to ideal targets reduced the risk of heart attack, stroke, heart failure, and cardiovascular death by 25 per cent. So, if your blood pressure is high, these lifestyle measures can help you to lower your blood pressure and give you a healthy head start in life.

The ABCs of high blood pressure

In most cases, diagnosis of high BP and hypertension should be made only after a period of evaluation

I recently saw a gentleman, Mr A, who had a history of frequent dizzy spells which were so severe that it made him unsteady when he was performing his activities of daily living. Mr A has been on high blood pressure (BP) medication for more than 20 years. After evaluation, his BP medicine was stopped, his dizziness resolved and his blood pressure remained normal.

Criteria for diagnosis

How should one determine that a person truly has high BP? According to the latest guidelines, an upper or systolic blood pressure (SBP) of 140 mmHg, and/ or a lower or diastolic blood pressure (DBP) of 90 mmHg on repeated examination in the clinic would meet the criteria of a diagnosis of high blood pressure or hypertension. In some patients with isolated systolic hypertension, only the SBP is elevated (140 mmHg) and the DBP is 90 mmHg.

This is more commonly seen in the elderly where there is decreased elasticity of the major arterial vessels due to age-related changes. The BP value that is used by doctors to determine whether someone has hypertension is based on the measurement of the BP while the patient is in the clinic. It is recommended that there should be two to three clinic visits between one and four weeks’ interval before a person is determined to have high BP and the diagnosis of hypertension should not be made solely on the basis of one single visit to the clinic.

However, the exception to this is when the BP on a single visit is 180/110 mmHg and there is also evidence from other evaluation that there is underlying heart disease, then the diagnosis of hypertension can also be made on a single visit. Should you be considered to have high BP, it is recommended that this should also be confirmed by repeated BP measurements at home.

The correct way of measuring blood pressure

The BP recording used by doctors is measured in a manner which is consistently observed so that it will be comparable. The optimal way to measure BP is to have a person seated with his back supported, his feet firmly on the floor, using a validated BP measurement machine or device on a table with his arm resting, and with the device at the mid arm at about the level of the heart. In addition, the cuff size must not be too big or too small and must be able to fit comfortably over the arm.

The room should be quiet and there should be no talking during and between the measurements. The person should be relaxed for three to five minutes and should have the bladder emptied before measuring the BP. In addition, there should be no smoking or consumption of coffee or caffeinated foods or exercise for 30 minutes prior to the measurement of BP. Once all these conditions are met, the BP levels can be taken and there should be an average of three measurements taken at one-minute intervals. It is advised that the average of the last two measurements be used as the BP recorded.

In the initial evaluation, it will be ideal to measure the BP in both arms. If there is a consistent difference between the two arms of more than 10 mmHg in repeated measurements, use the arm with the higher BP as the arm for routine BP measurement. If the difference is more than 20 mmHg, further investigation should be considered to look for an underlying cause. Generally, out-of-clinic BP measurements by patients at home or 24-hour ambulatory BP recordings prescribed by the doctors are more reproducible than the routine clinic measurements and are more closely associated with organ damage and related to high BP.

Hence, if your BP is elevated upon the visit to the clinic, it does not mean that you definitely have hypertension. Before a diagnosis of hypertension is made, it is advised that repeated BP measurements should be performed, done in a manner as described above and the BP validated with home measurements.

Types of hypertension

In addition to sustained hypertension which is the elevation of BP throughout the day, there are also individuals who have elevated BP values in the clinic but have normal BP values when they are measured out of the office or at home. This is termed white coat hypertension. These patients routinely present with high BP values at the clinic and if they are prescribed BP lowering medication, they may feel light-headed or dizzy at home as the blood pressure values can drop very low with the medication.

If their risk factor profile is low and there is no evidence of organ damage related to hypertension, medication is not necessary. However, they should be advised to manage this white coat hypertension with lifestyle modification. There is another category of patients with normal BP values in the clinic but the BP values are elevated at home. This condition is called masked hypertension. Unlike white coat hypertension, those with masked hypertension are at similar risk of complications as those with sustained hypertension and hence, they may need drug treatment to normalise the home BP readings.

Echocardiogram

One of the most useful tests to determine whether there is evidence of organ damage by hypertension is the echocardiogram, an ultrasound assessment of the heart. In patients with hypertension, the presence of high pressure in the heart chambers can result in a dilatation of the left upper heart chamber as the thinned walled chamber gradually distends as the BP increases. In addition, the muscular left lower chamber has to work harder to pump the blood out of the heart chamber to the aorta.

As a result of constant stress on the muscular left lower chamber, the muscles will become thickened. This is analogous to the increase in your arm muscle if you have to carry heavier and heavier weights. If the BP is very high in the clinic and the echocardiogram is normal, it is very likely that this patient has white coat hypertension and medication is unnecessary in the majority of these patients. In Mr A’s case, his persistently elevated clinic BP as a result of white coat hypertension prompted his doctor to keep increasing his BP-lowering medication till he was on multiple drugs. At home, the BP-lowering drugs resulted in a low BP causing him to have severe dizzy spells whenever he tried to change his posture.

Despite being diagnosed to have hypertension and having been put on BP lowering drugs for more than 20 years, his echocardiogram did not support the diagnosis of long-standing hypertension. Hence, the decision to stop all his BP medication “cured” him of his symptoms and yet allowed his BP to remain normal.

The take-home message here is that if you are suspected to have high BP, measure your home BP according to the optimal protocols described above before you resign yourself to a fate of taking medication for the rest of your life.