PLACE OF ORAL NITRATES IN MANAGEMENT OF IN-HOSPITAL POST MYOCARDIAL INFARCTION PATIENTS & IN EARLY OUT-OF-HOSPITAL TREATMENT.

( This will also apply for other acute coronary syndrome patients)

There are no clear criteria for use of oral nitrates in such patients and many junior doctors are confused about whether it is indicated or not.

Well, if the patient is undergoing primary PCI & There are no other flow-limiting lesions, then it is not certainly indicated.

Unfortunately, many of our patients do not have access to coronary angiograms for acute coronary syndromes.

My medical officers think that oral nitrates are given only for post-MMOCARDIAL infarction patients who have recurrent angina. If a post MYOCARDIAL infarction patient has recurrent angina, it is an indication for urgent angiogram and coronary revascularization rather than oral nitrates.

Simply, people should not blindly follow...........

 Treatment should be individualized based on the underlying pathophysiology.

Naturally, no one wants to experience the angina pain or discomfort again. It creates a lot of anxiety not only for the patients but also for whole family members.

As you all are aware acute coronary syndromes occur with a plaque rupture, resulting in an atherothrombotic process that occurs over a soft plaque, also called vulnerable plaque which has high lipid content & a high number of inflammatory cells.

Fortunately, the plaque healing & stabilization +/- regression is accelerated by high-dose statin which has revolutionized the treatment of coronary heart disease.

But this takes some weeks & we don’t want the patient to experience angina during those weeks.

Oral nitrates are converted to nitric oxide which is a powerful vasodilator, improves endothelial function, and has considerable antiplatelet action.

It reduces the episodes of coronary spasms at the atherothrombotic site and dilates the infarct-related artery increasing the ante-grade blood flow to the ischaemic area. It also dilates the normal coronary arteries increasing the collateral circulation to the affected area and improving capillary perfusion.

 By dilating the systemic veins and to a lesser extent systemic arterioles it reduces the oxygen demand to the heart muscles by reducing the workload due to the reduction of preloaded and afterload.

This certainly reduces the recurrence of post-acute coronary syndrome angina during the first few days & weeks while the plaque is healing. Not only that, but it also reduces the extent & severity of ischemia-related myocardial injury and dysfunction.

Once the patient becomes asymptomatic with good exercise tolerance, oral nitrates can be discontinued usually within a few weeks.

Oral nitrates are widely available, cheap, and free of major side effects. The major issue is headache due to vasodilation of cranial arterioles which can be controlled by dose adjustments.

What is preventing the widespread use of it, is the lack of proper understanding of underlying pathophysiology. Many junior cardiologists listen to the lectures in Europe where most patients undergo coronary angiograms & most flow-limiting lesions of major arteries are stented. Those patients don’t need nitrates.

We have to make it suitable for our community.

It is so sad that most junior cardiologists are mostly intervention-oriented oriented and many of them don’t even care about optimal medical treatment.

When I want to reduce my heart rate to around 55 in post-MI patients with preserved LV function & who have not undergone coronary angiogram, during my ward rounds, my all very senior medical officers still refuse to understand it and do not want to follow it for some unexplainable reason.

 They want to stick to no nitrates & minimal doses of beta blockers & ACEI which have no pharmacological values.

 They refuse to read as well!!!.

Shall catch up with you later on

“OPTIMAL MEDICAL TREATMENT OF POST-ACUTE CORONARY SYNDROMES INCLUDING ACUTE MYOCARDIAL INFARCTION “