Myocardial infarction, effect

Saito, K., Elce, J.S., Hamos, J.E., Nixon, R.A., 1993, Widespread activation of calcium-activated neutral proteinase (calpain) in the brain in Alzheimer disease a potential molecular basis for neuronal degeneration, Proc. Natl. Acad. Sci. U.S.A., 90, 2628—2632 Saido, T., Shibata, M., Takenawa, T., Murofushi, H., Suzuki, K., 1992, Positive regulation of p-calpain action by polyphosphoinositides, J. Biol. Chem., 267, 24585—24590 Sandmann, S., Yu, M., Unger, T., 2001, Transcriptional and translational regulation of calpain in the rat heart after myocardial infarction - effects of AT( 1) and AT(2) receptor antagonists and ACE inhibitor, Br. J. Pharmacol. 132, 767-777... 

V. Marangelli, C. Memmola, M.S. Brigiani, L. Boni, M.G. Biasco, D. Scrutinio, S. Iliceto and P. Riz-zon, Early administration of verapamil after thrombolysis in acute anterior myocardial infarction. Effect on left ventricular remodeling and clinical outcome. VAMI Study Group. Verapamil Acute Myocardial Infarction, Ital Heart J. 1(5), 336-343 (2000). 

K. W. Mahaffey, T.E. Raya, G.D. Pennock, E. Morkin and S. Goldman, Left ventricular performance and remodeling in rabbits after myocardial infarction effects of a thyroid hormone analogue, Circulation 91(3), 794-801 (1995). 

The dmg is effective in the treatment of ventricular arrhythmias, especially those following acute myocardial infarctions (1,2,22). 

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). 

In a more extensive international trial, 17,187 patients were treated intravenously with streptokinase alone, aspirin alone, a combination of streptokinase and aspirin, or placebo (78). Streptokinase and aspirin were equally effective in treating acute myocardial infarction, each decreasing mortahty by 25% their combination further reduced mortahty by 42%. A significant reduction in mortahty was seen even in those patients treated up to 24 hours after the onset of symptoms. 

Compared to streptokinase, urokinase has been less extensively studied because of its high cost, ie, about 10 times that of a comparable treatment with streptokinase. In addition to the indications described for streptokinase, urokinase is indicated for use in patients with prior streptokinase treatment, or prior Streptococcal infection. Urokinase is commonly used at a loading dose of 4400 units /kg, with a maintenance intravenous infusion dose of 4400 units/kg/h for thromboses other than acute myocardial infarction. In the latter case, a much larger dose, ie, 0.5—2.0 million units/h or a bolus dose of 1.0 million units followed by a 60-min infusion with 1.0 million units, has been found optimal (106). An intracoronary dose of 2000 units/min for two hours was used in one comparative study with intracoronary streptokinase (107). In this study, urokinase exhibited efficacy equivalent to streptokinase with fewer side effects. Other studies with intracoronary urokinase have adrninistered doses ranging from 2,000 to 24,000 units/min with a reperfusion efficacy of 60—89% (108—112). In another urokinase trial, 2.0 million units were adrninistered intravenously, resulting in a thrombolytic efficacy of 60% (113). Effectiveness in terms of reduction in mortaUty rate has not been deterrnined because of the small number of patients studied. 

Class IC antiarrhythmic drugs such as flecainide or propafenone block the Na+ channel (open state propafenone open and inactivated state) with a very long dissociation time constant so that they alter normal action potential propagation. Flecainide increased mortality of patients recovering from myocardial infarction due to its proarrhythmic effects (CAST study). Action potential is shortened in Purkinje fibres but is prolonged in the ventricles. 

Fondaparinux, the factor Xa-binding pentasaccharide (Arixtra, MW 1,728 Da), is prepared synthetically, unlike UFH, LMWH and danaparoid, which are obtained from animal sources. Despite only inactivating free factor Xa, clinical trials indicate that fondaparinux is an effective antithrombotic agent, both for venous thromboembolism prophylaxis and treatment, as well as for acute coronary syndrome and ST elevation myocardial infarction [4]. 

While epinephrine is usually well tolerated in young and healthy individuals, there may be problems in elderly patients with cardiac arrhythmia or previous myocardial infarction episodes [31-33]. Pharmacological effects of epinephrine include rapid rise in blood pressure, pallor, anxiety, tachycardia, headache and tremor as well as vertigo. Most commonly these effects occur after intravenous injection or after overdosing epinephrine. Cardiac arrhythmia or pulmonary edema may develop in serious cases [33, 34]. 

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]. 

Krumholz HM, Pasternak RC, Weinstein MC, et al. Cost effectiveness of thrombolytic therapy with streptokinase in elderly patients with suspected acute myocardial infarction. N Engl J Med 1992 327 7-13. 

HBD is a biochemical rather than electrophoretic assessment of the LD isoenzyme which is associated with heart. All five isoenzymes of LD exhibit some activity toward cx-hydroxy-butyrate as substrate, but heart LD shows the greatest activity. Serum HBD measurement is not as valuable as the electrophoretic determination of heart LD isoenzyme. High HBD activity has also been found in diseases of the liver. Rises associated with the hepatic effects of congestive heart failure can be disconcerting in the differential diagnosis of myocardial infarction. Wilkinson has used the serum HBD/LD ratio for the differentiation of myocardial disease from other disorders in which HBD activity is elevated, whereas Rosalki has not found the ratio to be helpful (39). 

Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) have been shown to improve vascular outcomes due to their cholesterol-lowering effects as well as multiple pleiotropic effects. In high-risk populations, statin therapy is known to reduce the risk of vascular events such as myocardial infarction and stroke. A meta-analysis of 10 trials involving 79,494 subjects showed that statin therapy reduced the incidence of stroke by 18%, major coronary events by 27%, and all-cause mortality by 15%. The SPARCL trial recently showed that high-dose HMG-CoA reductase inhibitors prevent recurrent stroke and transient ischemic attacks. ... 

Ticlopidine inhibits the P2Yj2 platelet ADP receptor, thus inhibiting ADP-dependent activation of the GP Ilb/IIIa receptor. It has a slow onset of action and takes 3-7 days to reach its maximal antiplatelet effect. It is inactive in vitro and must undergo activation by the hepatic cytochrome p450 enzyme system. Secondary prevention trials have found that ticlopidine-treated patients have an estimated RRR of 33% for the composite endpoint of stroke, myocardial infarction, or vascular death after ischemic stroke. Significant adverse effects include bone marrow depression, rash, diarrhea, and thrombotic thrombocytopenic purpura. No clinical trials have studied ticlopidine for the treatment of stroke in the acute phase. 

Cardiovascular Effects. In one case study, a woman who had accidentally consumed about 20 mL of trichloroethylene was reported to have suffered a myocardial infarction within 2 hours of ingestion (Morreale 1976). In two other case studies, men who ingested 350 and 500 mL of trichloroethylene had ventricular arrhythmias that persisted for up to 3 days (Dhuner et al. 1957). The arrhythmias were described as ventricular tachycardia with extrasystoles from different ventricular foci. Cardiac arrhythmia was also reported in a women who drank an unknown amount of trichloroethylene (Perbellini et al. 1991). 

Carotenoids and cardiovascular diseases — Numerous epidemiological studies aimed to study the relationship of carotenoids and cardiovascular diseases (CVDs) including coronary accident risk and stroke. It appeared then that observational studies, namely prospective and case-control studies, pointed to a protective effect of carotenoids on myocardial infarct and stroke, but also on some atherosclerosis markers such as intima media thickness (IMT) of the common carotid artery (CCA) and atheromatous plaque formation. 

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