Heart infarction

Minimal nitro-blue tetrazolium (NTB) unstained areas of the myocardium, indicative of minimal injury, are observed in hearts treated with CSIL at 5 min of ischemia (Fig. 3a, panel a). Myocardial injury increased with longer delays of CSIL treatment (at 10 and 20 min) (Fig. 3a, panels b and c). Hearts treated with IgG-L at 5,10, and 20 min ofischemia (Fig. 3a, panels d-f) show more extensive injury than the corresponding CSIL-treated hearts. Infarct sizes of hearts treated with IgG-L at 5, 10, or 20 min ofischemia (39 4%, 35 7%, and 45 6%, respectively) are the same (Fig. 3b). 

Damaged skeletal or heart muscle releases Ck. into the serum. Increases in serum Ck. are therefore used in the early diagnosis of heart infarction, the detection of muscle wastage, and to distinguish heart infarction from lung embolism, in which there is no increase in serum C. k. 

LDH is used for diagnosis of heart infarction and hepatitis, since its level in serum is considerably elevated in both these diseases. Purified LDH is used in coupled optical tests for the assay of other enzymes, e.g. pyruvate kinase, enolase, transaminases, and for the enzymatic determination of many metabolites, such as ADP, ATP, L-lactate and pyruvate. 

Bian GX, Li GG, Yang Y, Liu RT, Ren JP, Wen LQ, Guo SM, Lu QJ (2008) Madecassoside reduces ischemia-reperfusion injury on regional ischemia induced heart infarction in rat. Biol Pharm Bui 31 458 63... 

BIOLOGICAL ACTIVITY Antiinflammatory [7654-7659] antiarteriosclerotic agent [7641] atherosclerosis [7660] heart infarction inhibition [7661] antihypertensive [7662] antiallergic [7663],... 

Since on the other hand overweight is indirectly one of the risk factors of atherosclerosis, especially of heart infarction, it is of advantage to recommend a moderate intake of carbohydrates for the dietary prevention of coronary heart disease. This should be taken into consideration even if it would lack the final proof e.g. by epidemiological investigations for the importance of certain sugars in the pathogenesis of atherosclerotic disease. 

As you can see, in persons with one risk factor heart infarction and sudden death doubles, with two risk factors triples and in those with three risk factors these events are ten times more frequent, than in individuals who do not smdce and have normal (physiological) cholesterol and blood pressure values. 

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). 

Ventricular extrasystoles are treated only if they may degenerate into life-threatening arrhythmia. In milder forms the proarrhythmic risk of the diugs overshadows their benefits. In such cases (3-adrenoceptor antagonists may be attempted. For the treatment of ventricular extrasystoles, such as series or runs of extrasystoles, amiodarone or sotalol are used. In the absence of structural heart disease, class I anti-arrhythmic diugs can be considered an alternative. However, they may not be administered during the post-infarction period. 

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). 

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