Myocardial ischemia pectoris

The basic problem in angina pectoris is that the supply of oxygen to the heart is insufficient to meet myocardial demands at a given point in time, which results in an imbalance between myocardial oxygen supply and demand (Fig. 22—l).6 34 This imbalance leads to myocardial ischemia, which results in several... 

Although angina pectoris is believed to be caused by the buildup of lactic acid and other metabolites, the exact mechanisms responsible for mediating anginal pain remain unknown. Also, the emotional state of the patient and other factors that influence central pain perception play an obvious role in angina pectoris.20,34 In fact, the majority of anginal attacks may be silent in many patients, and myocardial ischemia may ffe-... 

Angina pectoris Severe pain and constriction in the chest region, usually associated with myocardial ischemia. 

Quiles J, Roy D, Gaze D, et al. Relation of ischemia-modified albumin (IMA) levels following elective angioplasty for stable angina pectoris to duration of balloon-induced myocardial ischemia. Am J Cardiol 2003 92 322-324. 

The major determinants of cardiac oxygen consumption are heart rate, myocardial wall tension (directly related to ventricular cavity pressure and volume) and force and velocity of contraction. Under normal conditions, the heart extracts oxygen at a near-maximal rate and added requirements are met by a reduction in coronary vascular resistance and an increase in blood flow. In the atherosclerotic heart, coronary vessels in the ischemic region and particularly in the subendocarium are already dilated and their ability to increase flow by further dilatation is severely compromised. Thus, under these conditions, increasing oxygen demand may exceed supply, myocardial ischemia ensues and the patient manifests symptoms of angina pectoris. 2... 

In a study using isolated guinea pig hearts, phthalide 20 exhibited negative chronotropic and inotropic responses and attenuated the decrease in coronary flow induced by pituitrin. This demonstrated the preload- and afterload-reducing properties of 20, which may contribute to its anti-anginal effect in vivo [305], This speculation, however, was challenged by the results in that 20 decreased the heart rate in renal hypertensive anesthetized rats [302] but its Z-isomer 22 did not affect the heart rate in normotensive conscious rats [303]. The impacts of phthalides 20 and 22 on cardiac function and angina pectoris/myocardial ischemia remain uncertain. 

The new millennium found lower extremity arterial disease (LEAD) and intermittent claudication in particular, pharmacotherapeutically orphan. Pharmacologically, intermittent claudication has been an orphan since it was first described many decades ago. Intermittent claudication, the cardinal symptom of LEAD occurs in 35 to 50% of patients with known LEAD documented by noninvasive diagnostic methods (1). The development of effective pharmacotherapy for treating claudication has lagged behind that for treating angina pectoris and other manifestations of myocardial ischemia. 

A similarly interesting case is that of a 68 year old male patient who was first seen in 1958 with symptoms of marked myocardial ischemia and electrocardiographic evidence of an old inferior myocardial infarction. Insulin dependent diabetes melli-tus had been present since 1932. In spite of diabetic control with diet and insulin in this subject, lipemia (approximately 2 gm neutral fat per 100 ml plasma) persisted and abdominal colics recurred. With heparin and later Depot-Thrombocid his neutral lipids ranged between 300—500 mg per 100 ml and clinical symptoms (angina pectoris and episodes of abdominal pain) improved considerably. An additional feature in this patient was gout with uric acid levels above 9 mg per 100 ml and attacks of acute gouty arthritis on several occasions between 1958 and 1959. 

The assessment of angina pectoris and myocardial ischemia has been facilitated by recent studies of catecholamine excretion, serum enz3 mes, antiheart antibodies,and myocardial serum lactic acid levels and arteriography. 

Chemical stimuli also underlie pain secondary to inflammation or ischemia (angina pectoris, myocardial infarction), or the intense pain that occurs during overdistention or spasmodic contraction of smooth muscle abdominal organs, and that may be maintained by local anoxemia developing in the area of spasm (visceral pain). 

Sildenafil was the first oral treatment for ED and is the most extensively evaluated (35). Overall success rates in patients with cardiovascular disease of 80% or greater have been recorded with no evidence of tolerance, Patients with diabetes with or without additional risk factors, with their more complex, and extensive pathophysiology, have an average success rate of 60%. In randomized trials to date, open-label or outpatient monitoring studies the use of sildenafil is not associated with any excess risk of myocardial infarction, stroke, or mortality (38-40), In patients with stable angina pectoris there is no evidence of an ischemic effect due to coronary steal, and in one large, double-blind, placebo-controlled, exercise study sildenafil 100 mg increased exercise time and diminished ischemia (41), A study of the hemodynamic effects in men with severe CAD identified no adverse cardiovascular effects and a potentially beneficial effect on coronary blood flow reserve (42), Studies in patients with and without diabetes have demonstrated improved endothelial function acutely and after long-term oral dose administration, which may have implications beyond... 

Vinca alkaloid-associated myocardial infarction, angina pectoris, and transient electrocardiographic changes related to coronary ischemia are limited to case reports (22-24). In addition, patients with these adverse effects... 

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