Heart Myocardial infarction

Atherosclerosis (athero = fatty and sclerosis = scarring or hardening) of the coronary and peripheral vasculature is the leading cause of morbidity and mortality worldwide. Lesions (called plaque) are initiated by an injury to endothelium and thicken the intima of arteries, occlude the lumen, and compromise delivery of nutrients and oxygen to tissue (ischemia). Atherosclerotic lesions primarily occur in large and medium-sized elastic and muscular arteries and progress over decades of life. These lesions cause ischemia, which can result in infarction of the heart (myocardial infarction) or brain (stroke), as well as abnormalities of extremities. The proximate cause of occlusion in these pathological conditions is thrombus formation. 

Fig. 4. Myocardial infarction occurs during insufficient delivery of oxygen to a portion of the heart muscle.

There is a close correlation between myocardial infarctions and tachyarrhythmias, illustrated by the presence of complex ventricular arrhythmias among heart attack victims which are estimated to affect one-third of the survivors each year. Frequendy, the immediate cause of sudden death is ventricular fibrillation, an extreme arrhythmia that is difficult to detect or treat. In the majority of cases, victims have no prior indication of coronary heart disease. 

Another example is the use of Tc-sestamibi, approved for use in the evaluation of coronary artery disease and myocardial infarction, in patients with breast cancer. Use in breast cancer is under investigation by a number of physicians. The data are not yet sufficient to determine the efficacy of this agent in this setting. Its safety, of course, has already been demonstrated as part of its initial evaluation for heart disease. 

Nitroglycerin remains the dmg of choice for treatment of angina pectoris. It has also been found useful for the treatment of congestive heart failure, myocardial infarction, peripheral vascular disease, such as Raynaud s disease, and mitral insufficiency, although the benefits of nitroglycerin in mitral insufficiency have been questioned. 

There can be a number of underlying causes of CHE. The most prevalent is the lack of oxygenated blood reaching the heart muscle itself because of coronary artery disease with myocardial infarction (111). Hypertension and valvular disease can contribute to CHE as well, but to a lesser extent in terms of principal causes for the disease. 

Other Cardiovascular Agents Effecting Atherosclerosis. A large amount of clinical data is available concerning semm Upid profiles in patients subjected to dmg therapy for other cardiovascular diseases. Atheroma, for example, may be the underlying cause of hypertension and myocardial infarction. There are on the order of 1.5 million heart attacks pet year in the United States (155). 

It is well accepted that hypertension is a multifactorial disease. Only about 10% of the hypertensive patients have secondary hypertension for which causes, ie, partial coarctation of the renal artery, pheochromacytoma, aldosteronism, hormonal imbalances, etc, are known. The hallmark of hypertension is an abnormally elevated total peripheral resistance. In most patients hypertension produces no serious symptoms particularly in the early phase of the disease. This is why hypertension is called a silent killer. However, prolonged suffering of high arterial blood pressure leads to end organ damage, causing stroke, myocardial infarction, and heart failure, etc. Adequate treatment of hypertension has been proven to decrease the incidence of cardiovascular morbidity and mortaUty and therefore prolong life (176—183). 

A third study (85) enrolled 7825 hypertensive patients (55% males and 45% females) having diastoHc blood pressures (DBP) of 99—104 mm Hg (13—14 Pa) there were no placebo controls. Forty-six percent of the patients were assigned to SC antihypertensive dmg therapy, ie, step 1, chlorthaUdone step 2, reserpine [50-55-5] or methyldopa [555-30-6], and step 3, hydralazine [86-54-4]. Fifty-four percent of the patients were assigned to the usual care (UC) sources in the community. Significant reductions in DBP and in cardiovascular and noncardiovascular deaths were noted in both groups. In the SC group, deaths from ischemic heart disease increased 9%, and deaths from coronary heart disease (CHD) and acute myocardial infarctions were reduced 20 and 46%, respectively. 

Indications for treatment with streptokinase include acute occlusion of arteries, deep vein thrombosis, and pulmonary embolism. Streptokinase therapy in coronary thrombosis, which is the usual cause of myocardial infarction (54,71,72), has proved to be valuable. In this frequently fatal condition, the enzyme is adrninistered intravenously at a dose of 1.5 million units over 60 min, or given by intracoronary infusion at a 20,000- to 50,000-unit bolus dose followed by 2000 to 4000 units/min for 60 min therapy must be instituted as soon as practicable after the diagnosis of heart attack is made. For deep vein thrombosis, pulmonary embolism, or arterial occlusion, streptokinase is infused at a loading dose of 250,000 units given over 30 min, followed by a maintenance dose of 100,000 units over a 60-min period. 

The complex investigation of the heart of IHD patients with Myocardial Infarction (MI) was performed. The results obtained showed that all investigated elements divided in two groups - the behavior in different parts of the heart of the certain elements (e.g., Se-Rb) were synergetic, the behaviour of another one was antagonistic (e.g., K-Ca, Fe-Br). 

In general, arterial thrombi are platelet-rich ( white clots ) and form at ruptured atherosclerotic plaques, leading to intraluminal occlusion of arteries that can result in end-organ injury (e.g., myocardial infarction, stroke). In contrast, venous thrombi consist mainly of fibrin and red blood cells ( red clots ), and usually form in low-flow veins of the limbs, producing deep vein thrombosis (DVT) the major threat to life results when lower extremity (and, occasionally, upper extremity) venous thrombi embolize via the right heart chambers into the pulmonary arteries, i.e., pulmonary embolism (PE). 

Myocardial infarcts Ca2+ homeostasis is lost in ischemic areas, triggering inappropriate calpain activity. Desmin and a-spectrin are degraded in ischemic hearts by synthetic calpain inhibitors. Protein and mRNA levels of m and (./-calpain increase after myocardial infarction40-43... 

Occurs when the volume of extracellular fluid is significantly diminished. Examples include hemorrhage, fluid loss caused by burns, diarrhea, vomiting, or excess diuresis Occurs when the heart is unable to deliver an adequate cardiac output to maintain perfusion to the vital organs. Examples include as the result of an acute myocardial infarction, ventricular arrhythmias, congestive heart failure (CHF), or severe cardiomyopathy. 

These dm are primarily used in the treatment of hypertension (see the Summary Drug Table Adrenergic Blocking Drugs also see Chap. 39) and certain cardiac arrhythmias (abnormal rhythm of the heart), such as ventricular arrhythmias or supraventricular tachycardia They are used to prevent reinfarction in patients with a recent myocardial infarction (1—4 weeks after MI). Some of these dm have additional uses, such as the use of propranolol for migraine headaches and nadolol for angina pectoris. 

Other contraindications for die anticholinergics include tachyarrhythmias, myocardial infarction, and congestive heart failure (unless bradycardia is present). 

These drugp are contraindicated in patients with known hypersensitivity to the drug or to any constituents of the drug, after a recent myocardial infarction (heart attack), or in patients with thyrotoxicosis. When hypothyroidism is a cause or contributing factor to a myocardial infarction or heart disease, the physician may prescribe small doses of thyroid hormone... 

MI myocardial infarction (heart attack) RF rheumatoid factor... 

An estimated oral dose of 260 mg endosulfan/kg caused severe seizures in a 43-year-old man, and brain death from cerebral herniation and massive cerebral edema occurred within 4 days of exposure (Boereboom et al. 1998) there were no signs of myocardial infarction and only slight congestion of the heart, but pulmonary congestion and atelectasis were evident at autopsy. 

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. 

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