The electrical conduction system that keeps the heart pumping.
WHEN I stepped into the cardiologist’s office for the first time, it was like getting behind the veil.
I had been having palpitations (atrial fibrillations) for about a year or so until one day they became uncomfortably persistent.
Thankfully, the cardiologist brought down my blood pressure (BP) which had shot up to 180/100, with a single tablet. The palpitations stopped for three days though my heart muscles felt sore – as if they had been overworked.
The echocardiogram revealed an enlarged left atrium, mild regurgitation of mitral valve, thickened left ventricular wall, and diastolic dysfunction (ventricular wall not relaxed enough so less blood was entering the left ventricle).
The diagnosis was hypertensive heart disease, the No. 1 cause of death associated with high blood pressure.
It refers to a group of disorders caused by high blood pressure that includes heart failure, ischaemic heart disease, hypertensive heart disease and left ventricular hypertrophy (excessive thickening of the heart muscle).
Heart failure means the heart’s pumping power is weaker than normal or the heart has become less elastic. With heart failure, blood moves through the heart’s pumping chambers less effectively, and pressure in the heart increases, robbing the body of oxygen and nutrients.
To compensate for reduced pumping power, the heart’s chambers respond by stretching to hold more blood. This keeps the blood moving but over time, the heart muscle walls weaken and are unable to pump as strongly.
As a result, the kidneys often respond by causing the body to retain fluid (water) and sodium. The resulting fluid buildup in the arms, legs, ankles, feet, lungs or other organs, is called congestive heart failure.
High blood pressure brings on heart failure by causing left ventricular hypertrophy, a thickening of the heart muscle that results in less effective muscle relaxation between heart beats. This makes it difficult for the heart to fill with enough blood to supply the body’s organs, especially during exercise, leading the body to hold onto fluids and heart rate to increase.
Symptoms of heart failure include shortness of breath, swelling in the feet, ankles, or abdomen, bloating, irregular pulse, fatigue and a greater need to urinate at night.
High blood pressure can also cause ischaemic heart disease. This means the heart muscle isn’t getting enough blood. Ischaemic heart disease is usually the result of atherosclerosis or hardening of the arteries (coronary artery disease), which impedes blood flow to the heart.
In order to treat hypertensive heart disease, the doctor has to treat the high blood pressure that is causing it with a variety of drugs, including diuretics, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers, angiotensin-receptor blocker (ARB) and vasodilators.
In addition, the doctor may advise changes to lifestyle, including lower daily intake of sodium if heart failure is present, eat foods high in fibre and potassium, limit total daily calories to lose weight and limit intake of food that contain refined sugar, saturated fat and cholesterol.
I was treated with an ARB and calcium channel blocker (both to dilate blood vessels and lower the BP) plus diuretic to reduce the blood congestion by getting rid of excess water. Later, an ACE inhibitor replaced the ARB.
After nine months of medication, I was still plagued by palpitations and was finally persuaded to try the Heart Hospital.
An echocardiogram taken at this hospital revealed that the nine months of treatment under the cardiologist had reversed my condition: the enlarged left atrium had shrank by 4 mm to a borderline 40 mm, mitral valve no longer leaks (though prolapsed), left ventricular wall no longer thickened, and no more dystolic dysfunction.
However the right atrium, like the left one, was enlarged to borderline size with traces of tricuspid valve regurgitation.
The doctor in the government clinic, on seeing the results, said my condition was not serious enough for referral to the Heart Hospital, so I opted for treatment at the clinic.
However, the ECG and echocardiogram had also revealed heart block.
The heart has two nodes instrumental in cardiac conduction – the sino-atrial (SA) node and the atrio-ventricular (AV) node. The SA node or pacemaker located in the upper wall of the right atrium generates nerve impulses that travel throughout the heart’s wall, causing both atria to contract.
The AV node lies on the right side of the partition that divides the atria, near the bottom of the right atrium.
Impulses generated by the SA node reach the AV node, where they are delayed for about a tenth of a second for the atria to contract and empty blood into the ventricles.
The AV node then sends the impulses down the atrio-ventricular bundle which branches off into two bundles and the impulses are carried down the centre of the heart to the left and right ventricles, causing them to contract.
If the electrical impulse initiated at the SA node takes too long to arrive at the AV node, it does not get through and the ventricles don’t contract, causing a missed beat.
In first degree heart block, atrial conduction is slow but no beats are missing whereas in second degree block, atrial conduction is too slow for the signal to get through, the ventricles don’t contract resulting in a missed beat.
In third degree block, no electrical signal gets through.
The first degree block I experienced occasionally descended into second degree block (with beats missing). I had been on a beta blocker for hypertension for more than 10 years and it had reduced my pulse rate to as low as 56 (normal 72 to 80).
Research revealed that beta blockers increase the refractory period at the SA node which slows down atrial conduction. They also increase the refractory time of the AV node, slowing AV conduction.
Doc put me on an ACE inhibitor with least effect on heart rate, a calcium channel blocker with high bioavailability and a diuretic.
The ACE inhibitor induced coughing and a lip ulcer, so was withdrawn on the fifth day. Kinins deposited in the lungs as by-products from the use of ACE inhibitors were said to be responsible for causing the hacking cough.
In my case, the coughing was found due to infection of the lungs by super bugs, and it was cured with a strong antibiotic.
The palpitations were reduced though I noticed that they could be triggered by food containing preservatives such as sodium benzoate or boric acid, high cholesterol, poor diet or long periods without food.
According to research, boric acid is a poison which, among others, is used to kill fungus, viruses and cockroaches but is being used to increase the shelf-life of certain foodstuff.
Meanwhile, sodium benzoate is a permitted food preservative used in low concentrations in certain food. I found sodium benzoate in certain brands of soya sauce, tomato sauce and chilli sauce.
According to research, sodium benzoate can starve the cells of oxygen, and it affects the mitochondria in the DNA. Thus, sodium benzoate, coupled with a drug-induced depressed heart rate, could reduce the amount of oxygen supplied to the brain – which affects concentration and memory – besides the rest of the body.
Sodium benzoate produces benzene in the presence of Vitamin C like fruit juices, and benzene can cause cancer.
It appears nutrition (balanced diet, reduced salt and sugar intake, no preservatives), lifestyle changes (reduce stress), exercise and weight loss hold the key to the long-term cure for hypertension.
For now, my BP is being stabilised by low doses of an ACE inhibitor, calcium channel blocker and diuretic, taken twice a day.
The palpitations inevitably point to the damage hypertension has done to my heart, which was fortunately reversible. I thank God, my cardiologist, doctors, pharmacist, senior medical assistant, church elders, pastors, colleagues and acquaintances.