Unstable Angina

Unstable angina

     Unstable angina term was first used three decades ago and means intermediate status between myocardial infarction and the chronic stable angina. Unstable angina is synonymous with the terms intermediate syndrome and pre myocardial.

     The incidence of unstable angina is growing and nearly one million people receive this diagnosis. Risk of death, myocardial infarction and various complications is due to varied clinical spectrum which is covered by the term unstable angina. Studies show that the incidence of death in the first week after admission is 4% and the incidence of myocardial infarction is 10%. Negative prognostic factors are: old age, left ventricular dysfunction and enlargement of the disease.

     Women with unstable angina are old and have a high prevalence of hypertension, diabetes, congestive heart failure and a family history of heart disease richer than men. Men tend to present high incidence of myocardial infarction and revascularization, increased levels of cardiac enzymes and high rates of diagnostic catheterization and revascularizations. The prognosis is still more dependent on the severity of the disease than sex. The average age of presentation of patients is 62 years. Women are 5 years older than this at diagnosis.

     Unstable angina causes are the same as for the stable one: breaking a buildup plaque with the formation of thrombus which completely or partially obstructs a main coronary branch, severe anemia, hypertension and congestive heart failure.

     Unlike stable angina, pain or discomfort associated with unstable angina:

• Often occurs at rest, sleep at night or minimum physical activity
• Is suddenly, is severe and lasts more than 30 minutes
• Is not relieved by rest or nitroglycerin
• Is a sign that predicted an attack in the near future.

     For people with unstable angina the treatment options are immediately, to prevent cardiac infarction. In over 85% of patients, the emergency treatment will stabilize the symptoms. You may opt for a catheterization, angioplasty or cardiac bypass. Emergency angioplasty and open heart surgery are necessary to the patients who don't respond to the remaining methods.

Pathogenesis of unstable angina

     Unstable angina is derived from the common pathogenesis due to ischemic heart syndromes. Typical outburst of unstable angina is the rupture of the buildup plaque with rapid formation of thrombus with secondary hemodynamic deficiency. Unstable angina is etiological different from stable angina which is caused mostly by a fixed coronary stenosis which compromises the blood flow.

     The factors that interfere in the pathology of unstable angina include: demand-supply imbalance in myocardial oxygen, rupture of the buildup plaque, thrombosis, vasoconstriction and blood flow cyclically.

Demand-supply imbalance for myocardial oxygen

     Myocardial ischemia from unstable angina results from the excessive or improper application of oxygen, glucose and free fatty acids. Diseases that cause secondary ischemia are the ones by increasing the O2 demand of myocardial (cocaine, severe illnesses, psychological stress) or by decreasing the intake of O2 (anemia, hypoxaemia, and hypotension).

Breaking the buildup plaque

     The accumulation of macrophage filled with fat and smooth muscle cells is the base event on buildup plaque formation. Oxidation of LDL-C in aerated cells is cytotoxic, chemotactic and pro coagulant. Increased plaque instability associated with impaired blood flow and vascular wall stress leads to cracking or breaking the plaque. The minor cracks are non occlusive and asymptomatic. Moderate to large plaque ruptures lead to unstable angina or myocardial infarction.

Vasoconstriction, vasospasm and cyclic flow of blood

     Most patients with acute coronary syndrome shows reduced blood flow due to the appellant transient vasoconstriction and clot formation at plaque rupture. These events occur because of episodes of platelet aggregation and complex interaction between vascular wall, leukocytes, platelets and atherogenic lipoproteins.