The Heart Centre, Lajpat Nagar, Delhi
Friends, it is really a great honor and privilege me to be here this morning and interacting with a very eminent cardiologist, not only of India but of the whole world. He is Prof. M. Khalilullal. I do not think he needs an introduction here. He is a very eminent person, he is a pioneer or father figure electrophysiology and he is considered as the father of cardiology in today’s world in India at least. I know him for last almost 45 years when I was a student in a medical college. The only person I knew from Delhi were only two, Padmavathi and Dr. Khalilullal and I am very privileged that here I am interacting with him on a very important issue today. Dr. Khalilullal, I think there is a lot of data coming up that we see a lot of hypertrophy of the heart these days and these people either have hypertension or they have hypertrophic cardiomyopathy. I like to have your viewpoints, LV hypertrophy, which we see because of hypertension, what is the comorbidity associated so that our students or our PGs can get a message of a hypertrophic cardiomyopathy and a hypertrophy produced by hypertension if not controlled meticulously. Your viewpoints sir.
The ventricle has got two functions to perform. One is systole, a contraction so we can push the blood to the entire body to provide with nutrition and oxygen etc. etc., and the other function is diastole, it is relaxation. The ventricular hypertrophy interferes with the relaxation part of the heart, the diastolic function and thereby the flow of blood coming to the heart is impeded and there is a back pressure from there on to the proximal chamber of the heart which is the atrium and from there on to the lungs on the left side on the right side to the vena cava, etc. So when the hypertrophy takes place because of hypertension, it is gradual and it is usually in the free wall, but the hypertrophy of the hypertrophic cardiomyopathy takes place, it is the hypertrophy in the septum. The septum gets hypertrophy apart from the free wall and that cause obstruction to the outflow tract, also when the ventricle context, it finds that there is an obstruction outflow tract with the gradient across the left ventricle cavity and the aorta. The gradient is below the aortic valve, it is a dynamic gradient like when the patient stands up suddenly there is a decrease in the ventricle filling and the gradient will increase, when the patient lies down it will decrease. It can increase remarkably on exercise. So, it is very important to know that the people who have hypertrophic cardiomyopathy have big risk of developing high gradient in the left ventricle because of exercise. On the other hand of diastolic function is a phenomenon which occurs all through. It can be aggravated by exercise because the cardiac output increases from a routine of 5 liters to about 8 or 9 or 10 liters depending upon the vigorous exercise you are performing and the inflow of the blood coming to the heart and the heart is not able to relax, not able to diastole and could not get into the good diastolic function then the back pressure can take place and the pressure can rise on the left side of the heart. The left atrium starts getting dilated and there is pulmonary congestion. The patient gets. Another very important factor which leads to a prolonged left ventricular hypertrophy is the atrial dilation and arrhythmia of which atrial fibrillation is a very, very important phenomenon which is associated with high degree, high insidious stroke. A person who looks otherwise normal has hypertension and has left ventricular hypertrophy and has left ventricle dysfunction and left ventricular dilatation and stroke can suddenly get into disabled situation and I think his career is totally at a stake and his life at a stake. So, left ventricular hypertrophy should not be taken lightly, should be taken with all vigorous attention and now we have been talking about the heart failure with preserved LV systolic function. Now, there is a phenomenon which is now gradually picking up. It is different to treat the systolic dysfunction, requires a lot more attention and a little light in line of therapy.
I think Prof. Khalilullal has given an address to a very complex issue in a very simplified manner for our proper understanding. Dr. Khalilullal said that LV hypertrophy is very, very important. We should not underestimate or ill-understand or not understand the significance of LV hypertrophy. We must give due respect to LV hypertrophy and he is very categoric. He said the hypertrophy of LV produced by hypertension can be a concentrically hypertrophy or a generalized LV hypertrophy, it can be eccentric or it can be a concentric remodeling. It may not be a hypertrophy. It can be just a change which is remodeled. These are the three important things which can help her in the hypertension and they do not affect the hemodynamics of the left ventricular outflow tract significantly usually and he is very specific. He said the hypertrophy produced in a hypertrophic cardiomyopathy is usually asymmetric. There can be a bit cavity obstruction, there can be LV outflow tract obstruction and he also said that all these patient’s are more vulnerable to go even to a sudden death and he said very categorically that it is purely physical exercise dependent or a heart rate dependent, more the tachycardia more the chances of more obstruction in the LVOT or in the mid cavity and more chances of sudden cardiac death, which we usually do not see with the hypertrophy of heart produced by the hypertension and Dr. Khalilullal has mentioned very clearly that the hypertrophy should be prevented, regressed, or reversed by all the methods possible to reduce the vulnerability for arrhythmias to reduce the damage in the microvasculars, so that we are producing less damage to the heart or the vessels, so there is a less vulnerability for a heart attack and he also said we can also reduce the prevalence of sudden cardiac death and atrial fibrillation. He is focusing on atrial fibrillation. All these patients who are hypertensive with LV hypertrophy have increased pressures in the LV end diastole as well as increased LA pressure, LA size increase, more atrial fibrillation and he said that they are more vulnerable to get a stroke. So, it is multimodality. I think it is multifactorial and it has got a multi-morbidity, so this should be prevented, regressed and reversed aggressively if he really wants to reduce the morbidity and mortality produced by uncontrolled hypertension. Prof. Khalilullal, I think your words of wisdom are very well taken and I think the way you mentioned about the cardiomyopathy which is very different entity and he used the word asymmetry and he also said something on the aorta that it can be mid systolic occlusion of the aortic valve which may also affect and he also said asymmetric hypertrophy what we call ASH and he also says that there can be some abnormality in the mitral valve what we call as SAM, systolic anterior motion of the mitral leaflet. All these are obstructive or hemodynamic changes, the hemodynamic changes are very, very fast in hypertrophic cardiomyopathy and usually it is familial, friends and families where there are sporadic cases are also known and the treatment is very different. I think Prof. Khalilullal’s message is very clear that the hypertrophy of the heart should not be taken easily. Sir, my important question to you is that we do a lot of lifestyle modification and we give some drugs like beta blockers or calcium channel blockers, ACE inhibitors or ARBs and there are a lot new drugs coming up now. Do you think that will really reverse the hypertrophy, regress the hypertrophy pharmacologically and nonpharmacologic methods as compared to a hypertrophic cardiomyopathy sometimes they are to go for a radiofrequency ablation or a surgical myomectomy or of course we use the drugs, they are also. We would like to have your viewpoint on that. Since you are an EP man of the world, we would like to have your clear cut delineation of hypertrophic heart because of hypertension and hypertrophic heart because of hypertrophic cardiomyopathy and the modality for approach.
I think hypertrophy of the heart because of hypertension can be regressed by virtue of lifestyle modification, cutting down salt intake, controlling of blood pressure, fall in yoga, meditation and destressing yourself to cut down the surge of catecholamine body and weight loss, etc., as well as by the whole range of pharmacological interventions available to us lifelong beta-blockers to ACE inhibitors, ARBs, or combinations. This all do not happen and that is why I was describing in the earlier interview that we should keep a watch on this situation by doing an echocardiogram at least once in six months, get to a bit of time, but in patients who have hypertrophic cardiomyopathy, the situation is different. It could lead to vascular dysfunction and dysfunctional congestive heart failure can lead to arrhythmia and sudden cardiac death. It has been now tried to regress septal hypertrophy by several techniques one is in the cath lab you can do alcohol septal ablation, you can do septal artery and the branch of the LAD and inject alcohol, block it up thereby cause a controlled necrosis of the septum and thereby decrease the outflow obstruction. The other thing is radiofrequency technique, but I think what has been now proved beyond doubt that long-term survival patients who undergo myomectomy is possibly better than all these techniques, still the incidence of sudden cardiac death can or cannot be modified by all these techniques; therefore, implantable cardioverted defibrillator is indicated in some of these patient in whom you are documented lethal ventricular arrhythmias is very important.
It was very well explained by Prof. Khalilulla that the treatment of hypertrophic cardiomyopathy is very, very different as compared to what we see in the hypertrophy with the hypertension and he said that there has been some controversy initially of alcohol septal ablation and septal ablation by radiofrequency and myomectomy. The data is more in favor of myomectomy to have a long-term benefit because the short-term benefits are definitely seen with the septal ablation with th alcohol or with the radiofrequency and he also said the number of these patient’s are more vulnerable to go into ventricular ectopics. So, there is a postectopic gradient and they are more vulnerable to a sudden death, to use the word ICD. We have to use ICD (intracardiac device) as defibrillator, so that we prevent the death, very important message and there is a huge data, a lot of patients you know because he said in his first statement that when these patients stand, the gradient becomes very high and especially if this is an ectopic may be ventricular ectopic, the gradient becomes further high, the chances of sudden death are very high. The only way you can prevent by a device, which I think Prof. Khalilulla is very categorically mentioned. I think the message is very clear by Dr. Khalilulla’s word of wisdom that hypertrophy of heart because of hypertension should not be taken easily.