CARDIOLOGY KEY POINTS

Q- Why Left Ventricular Hypertrophy Occur? The mechanism of ventricular hypertrophy in patients with hypertension is as yet uncertain; however, activation of the renin-angiotensin-aldosterone system (RAAS) as a result of myocardial stretch and other factors is recognized as playing an important role. Angiotensin II has been shown to stimulate various growth factors, cytokines, fibroblast activity, myocyte hypertrophy, and myocardial fibrosis (t belongs to a class of diseases collectively known as fibrosis, which denotes hardening or scarring of tissue.) . Strategies to prevent activation of the RAAS and/or its effects would therefore appear attractive in preventing ventricular hypertrophy and its consequences in patients with hypertension. ACE inhibitors increase nitric oxide release and reduce morbidity, ischemic events, and mortality in patients with heart failure, including those with a history of hypertension. Q- Which types of patients benefits more with beta blockers? Finally, beta- blockade remains very important in the treatment of cardiovascular diseases, and in hypertensive patients with coexisting angina. Further, hypertensive patients younger than 50 years old may benefit more from beta blockage than older patients as they have different hemodynamic form of hypertension. Q- Are newer beta blockers which have vasodilator properties better than traditional one? Beta blockers which reduce heart rate but increases central aortic pressure and aortic pulse pressure are less beneficial as compare to those which reduces heart rate and decreases aortic pressure and aortic pulse pressure like carvediolol and Navelol. Q- At the dose of 50mg OD, what is the affinity of Atenolol for Beta 1 and Beta2 receptors? Its affinity is 80% for Beta 1 receptor and 20 % for beta- 2 receptors. Q- Atenolol treatment leads to similar blood pressure reduction as with other antihypertensives but arm receiving Atenolol has high all cause mortality. Why? 1. Atenolol differs from other beta blockers in its low lipophilic profile. Animal studies suggest that the ability to prevent ventricular fibrillation depends on the amount of beta blocker in the central nervous system, with the hydrophilic atenolol having very low permeability into the nervous system. 2. Beta blockers seem to have less beneficial effect on regression of left ventricular hypertrophy than other antihypertensive drugs (specially ACE inhibitors).

3. Many antihypertensive drugs correct the remodeling and endothelial dysfunction of small arteries seen in hypertension, but this has not been observed for atenolol. In a recent study, when patients on atenolol were switched to an angiotensin-1receptor blocker, the arterial media/lumen diameter of resistance arteries decreased and endothelium-dependent relaxation increased.