Prinzmetal Angina


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Prinzmetal Angina

Prinzmetal angina


     Prinzmetal angina or vasospastic angina is a special form of unstable angina through coronary spasm that causes acute transmural ischemia with transient ECG alterations of infractoid type.

     Prinzmetal angina spasm is a sudden contraction, with a particular temporary location in myocardium proper to a coronary. Spasm slows or stops the blood flow through arteries and deprives the heart of O2 and nutrients. Prinzmetal angina may occur in arteries that appear normal or those which have become calcified due to atherosclerosis. Coronary artery spasm is a cause of cardiac ischemia, and affects about 4 in 100. 000 persons and 2% in patients with angina (prinzmetal angina).

     Spasm can be silent with no symptoms or may occur in people with stable angina, or unstable. Usually appears as prinzmetal angina, a type of chest pain that seems to be determined by endothelial dysfunction, a pathologic condition that may occur with normal coronary arteries but does not work optimally.

     Prolonged prinzmetal angina may even cause heart attacks.

     Factors that trigger the coronary spasm are: alcohol, strong emotions, exposure to cold and medications that cause vasoconstriction. Cocaine and smoking can cause severe coronary spasm by increasing the heart labor. In many people prinzmetal angina can occur without any obvious cause.

     The main symptom is angina at rest, spontaneous, intense, prolonged (10, 15 minutes) occurred in the early morning hours, possibly with a fixed timetable. Usually exercise capacity is maintained. Other accompanying signs and symptoms are: feeling of chest pressure, the claw, suffocation, crushing. The pain is severe and may radiate to neck, shoulder or arm. Affected person may lose consciousness.

     Tests needed to diagnose prinzmetal angina include: coronary angiography and ECG's.

     The goal of treatment is to control pain and prevent heart attacks. Vasodilator nitroglycerin is the main agent used in prinzmetal angina. Calcium blocking is extremely effective in prinzmetal angina from stable angina. Combination with nitrates is beneficial. It can be associated two calcium blocking.

     Prognosis is favorable. 3 years survival rate ranges between 84-98%. Mortality is dependent of atherosclerotic disease. Patients without stenosis 70% have a 93% survival rate at 1 year, while those with multi vascular coronary atherosclerotic disease and prinzmetal angina have only 65% likely to survive to 1 year.


Pathogenesis of prinzmetal angina


     Prinzmetal angina is caused by coronary artery spasm, focal and general abnormality of the coronary arteries. Focal artery spasm usually appears in place of a stenosis or adjacent to it. A large number of patients show a normal coronary angiogram, although they demonstrated evidence of atherosclerotic disease by intravascular ultrasound examination.

     Nitric oxide is a potent endothelial relaxing factor responsible for maintaining coronary vasodilatation in the relative stage. Nitric oxide is synthesized locally in the amino acid L-arginine and catalyzed by the nitric oxide synthase. Nitric oxide is responsible for inhibiting platelet adhesion, activation and their aggregation. Activated platelets are responsible for the release of potent vasoconstrictors factors, including thromboxane A.

     Nitric oxide synthase dysfunction and reduced bioavailability of nitric oxide can cause a reduced basal vascular tone, vasoconstriction, vasospasm and activation, platelet aggregation and adhesion to the release of vasoconstriction secondary factors. Increased serum LDL, especially oxidized form is responsible for the decreased production of nitric oxide synthase by down-regulation of NO and oxidative inactivation of NO by frees radicals of O2.

     Coronary spasm in the prinzmaetal angina occurs at an atherosclerotic stenosis or its vicinity on endothelium which shows fat striations or fibrous plaque.


Risk factors for prinzmetal angina


     Factors that may trigger a crisis of prinzmetal angina include:

  • Old age, familial aggregation through polygenism as well as through food habits
  • Dietary factors: excessive caloric intake, water consumption last
  • Obesity
  • Smoking
  • Lack of exercise, emotional stress and professional
  • Diabetes, hyperuricemia, dyslipidemia
  • Hypertension, which increases coronary parietal stress.

     The combination of the three major risk factors (hypertension, diabetes, high cholesterol) increased by six times morbidity compared with subjects which presents a single risk factor.