Acute myocardial necrosis

Cardiac toxicity can be observed at high doses of cyclophosphamide (usually over 1.5 g/m /day), and acute myocardial necrosis or severe cardiac failure have been anecdotally reported after smaller dosages (SEDA-21,386). 

The authors concluded that even if beta2-adrenoceptor agonists can cause myocardial ischemia in pregnant women by further increasing oxygen consumption, acute myocardial necrosis is rare however, in this case... 

In the second scenario, the test result excludes a diagnosis this is referred to as a rule-out test. The actions resulting from excluding a diagnosis will invariably involve the evaluation or creation of another hypothesis. When a patient is admitted with atypical chest pain and acute myocardial infarction is suspected, the measurement of troponin maybe used to rule out (or rule in) acute myocardial necrosis. 

Acute myocardial necrosis 90-120 min after intravenous injection of Tc(tin)-pyro-phosphate... 

A 39-yeat-old female asthmatic took isoprena-line (1 200) by inhalation several times each hour because it provided only transient relief of dyspnoea. She took in all 675 mg in less than 3 days and was admitted in acute respiratory distress heart rate was 120/minute, blood pressure 230/160 mm Hg and respiratory rate 40/minute. She responded to hydrocortisone but ECG and serial enzyme changes were consistent with acute myocardial necrosis (3 ). 

Wagner et. al (46) studied 376 patients to evaluate the importance of identification of the myocardial-specific MB isoenzyme in the diagnosis of acute myocardial infarction. An attempt was made to determine the incidence of falsely positive (mb). No acute infarction was diagnosed in all patients in whom neither total CK nor the isoenzymes of LD indicated myocardial necrosis. Incidence of falsely negative (MB) was zero in 33 patients. They concluded that determination of the isoenzymes of CK provides both a sensitive and specific indication of acute myocardial infarction. 

The observation that the agent accumulated in necrotic tissue and not specifically or preferentially into viable tumors led to the investigation of the agent as a marker for necrosis [110]. Acute myocardial infarctions were induced in rats... 

Based on a retrospective study of 344 patients with cocaine-associated chest pain, it has been suggested that patients who do not have evidence of ischemia or cardiovascular complications over 9-12 hours in a chest-pain observation unit have a very low risk of death or myocardial infarction during the 30 days after discharge (59). Nevertheless, patients with cocaine-associated chest pain should be evaluated for potential acute coronary syndromes those who do not have recurrent symptoms, increased concentrations of markers of myocardial necrosis, or dysrhythmias can be safely discharged after 9-12 hours of observation. A protocol of this sort should incorporate strategies for treating substance abuse, since there is an increased likelihood of non-fatal myocardial infarction in patients who continue to use cocaine. 

The main reason is that the need for preconditioning cannot be foreseen. Acute myocardial infarction most frequently strikes unannounced. Thus, the application of preconditioning usually cannot be pre-ordered at will. Indeed, a body of evidence has accumulated that pre-infarction angina, which comes as close to preconditioning as possible, can be protective as regards limiting myocardial necrosis and protective against ventricular arrhythmias.4 10... 

Anteroseptal versus inferolateral MI prognostic implications. It is known that the MI involving LAD presents for similar area of necrosis, increased myonecrosis, reduced early and late left-ventricular function and high mortality compared with infarction in other vascular territories. However, the mechanisms underlying a worse prognosis are not completely characterised. Recently, it has been demonstrated (Kandzari et al, 2006) that prognosis after primary PCI in patient with ACS, the majority with ST-segment elevation, is different in patients with LAD occlusion than in RCA or LCX. Acute myocardial infarction due to LAD is associ-... 

The importance of other factors additional to amount ofnecrosis has also been studied. In patients with first acute MI treated with PCI, LAD-related MI show for a similar amount of myocardial necrosis as determined by enzymatic infarct size, lower left-ventricular ejection fraction (LVEF) when compared to non-LAD-related MI. LVEF-measured 6-month post-MI showed a decrease, for every 1000 cumulative lactate dehydrogenase release, of 4.8% for LAD and 2.4% for non-LAD-related infarcts (p < 0.0001), and these results remain in the multivariate analysis (Elsman et al., 2006). 

Hendel, R. C., McSherry, B. A., and Leppo, J. A. (1990) Myocardial uptake of indium-ill-labeled antimyosin in acute subendocardial infarction clinical, histochemical and autoradiographic correlation of myocardial necrosis. J. Nucl. Med. 31,1851-1853. 

Thrombolytics are dmgs that promote the fibronolytic mechanism if administered within 4 hours following an acute myocardial infarction (AMI). An acute myocardial infarction (heart attack) can be caused by a thromboembolism blocking a coronary artery. This results in decreased circulation to that part of the heart. The ischemic (without oxygen) tissue becomes necrotic (dies) if left without an oxygen supply. Thrombolytics prevent or minimize necrosis that results from the blocked artery and therefore decreases hospitalization time. After thrombolytic treatment, the patient is evaluated for cardiac bypass or coronary angioplasty procedures. 

Acute myocardial infarction can be limited by streptokinase which dissolves fresh clots and opens the artery, but muscle death and necrosis causes a mechanical defect. Subsequent infarcts cause further muscle death and ultimately lead to defective ventricular function and cardiac failure. There is the need for simple alarm systems to detect acute myocardial infarction and less traumatic invasive procedures to dissolve the clot and dilate the artery immediately. Coronary arteries ramify and branch in 3-dimensional space and the present generation of balloon catheters for percutaneous transluminal coronary angioplasty carries a small but definite risk. New, non-traumatic guidewires, low profile dilatation systems and more powerful dilatation balloons which will not rupture the artery are needed. 

The answer h3[IVA 2], Monensin, an ionophore, causes acute cardiac effects by interring with calcium and sodium transport Elevated intracellular calcium levels impair mitochondrial respiration, resulting in significant myocardial necrosis. The damaged myocardium is repaired by fibrosis ich lea to cardiac muscle insufficiency, exercise intolerance, and sometimes sudden death in survivors of acute rtxuiensin toxicosis. 

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