Angina Pectoris

ANGINA PECTORIS is a clinical syndrome due to transient myocardial ischemia caused by an imbalance between myocardial blood supply and oxygen demand. Myocardial oxygen demand actually exceeds oxygen supply. It comes from the latin words: "Angere" meaning "to choke" and "Pectus" meaning "chest".

Angina Pectoris has a wide range of clinical symptoms but the most common complaint described by patients is a squeezing, central, substernal chest pressure or tightening most often radiating to the arms, shoulders or jaws.

The most common clinical sign observed in patients is the clutching of the patient's chest or what we call as Levine Sign.

There are several variants of Angina Pectoris and they include the following:

1. STABLE ANGINA PECTORIS - a state of cardiac condition wherein anginal symptoms repeatedly occur during physical exertion. This is most probably caused by inadequate oxygen delivery to myocardial tissue due to a narrowed coronary artery. Since physical exertion demands oxygen and blood supply, the narrowed coronary artery provides a cumulative effect on the decreased oxygen and blood supplied to the myocardium.
2. UNSTABLE ANGINA PECTORIS belongs to the spectrum of clinical presentations collectively known as Acute Coronary Syndrome or ACS. This syndrome includes the ST segment Elevation Myocardial Infarction (STEMI) and the Non-ST segment Elevation Myocardial Infarction (NSTEMI). This type of angina is considered as a state wherein there is noted myocardial ischemia without apparent myocardial necrosis thus cardiac biomarkers of myocardial necrosis such as creatinine kinase MB isozyme, troponin and myoglobin are expectedly not noted in the circulation.
3. PRINZMETAL ANGINA OR VARIANT ANGINA is noted upon transient coronary artery spasm occurence. The spasms may be noted either at rest or with physical exertion but these spasms are not associated with pathological plaque or deposition within the coronary arteries. If an angiography is done, the coronary arteries usually appear normal while still noting spasms.
4. CARDIAC SYNDROME X is the presentation of all the anginal symptoms in patients without the presence of either a coronary artery disease or coronary spasms.

PATHOPHYSIOLOGY

In understanding the pathophysiology of myocardial ischemic syndromes, we need to recognize the primary dysfunction in Angina Pectoris and that is decreased oxygen delivery to myocardial muscle cells. 

There is 2 main mechanism that impairs delivery and that is coronary artery narrowing and endothelial dysfunction while the other mechanism impeding oxygen delivery usually exacerbate the symptoms:

1. Coronary Artery Narrowing - this accounts for the underlying reason for the cardiac ischemia in majority of cases as even a small change in the diameter of a blood vessel may be profound and detrimental to the patient. This may be dictated by application of the Poiseuille Law which states: "the rate of flow is decreased exponentially by any change in the radius of the lumen". There may be a significant decrease of blood flow rate as much as one half (1/2) for those with blood vessel lumen narrowing by one fifth (1/5th) thereby directly affecting oxygenation for the cardiac muscle region supplied. Angina is postulated to occur when compensatory mechanism of epicardial vessels to dilate (via the autoregulatory response) to respond to increased demand is overwhelmed.
2. Endothelial Dysfunction - Endothelial factors are noted to have significant roles in angina pectoris especially during sympathetic stimulation - the endothelium is influenced by mediators of both vasoconstriction and vasodilation. A quick review of these mediators shows that Alpha-Agonists (Catecholamines) causes vasoconstriction while Nitrous Oxide (created by endothelial nitrous oxide synthase) causes the counteraction of vasodilation. So what happens in diseased coronary artery is - there is ABSENCE or REDUCTION of Nitrous Oxide production thereby overwhelming the autoregulatory response and resulting to further blood vessel constriction.

So the Coronary Artery Narrowing which reduces blood flow rate added to further vasoconstriction caused by Nitrous Oxide production reduction and no counteraction of Alpha-Agonist (Catecholamine) effects mainly causes the overall impediment of oxygen delivery to myocardial muscle cells.