Cardiac enzymes

It is important to obtain a baseline EKG and cardiac enzymes to evaluate the possibility of an acute myocardial infarction. The short-term (2-4 weeks) stroke risk after acute myocardial infarction (AMI) is 2.5%. Stroke is usually an early (within 14 days) complication of AMI and is more common in anterior wall (4—12%) than in inferior wall infarction (1%). Approximately 40% of patients with an anterior wall myocardial infarction develop left ventricular thrombus. 

Given to patients with a history of typical angina accompanied by either a past medical history of coronary artery disease or ECG/cardiac enzyme changes, low molecular weight heparins (LMWH) were more efficacious in reducing MI and revascularization, but not mortality, with fewer serious side-effects than unfractionated heparin (UFH) (see Magee et al., 2003). 

Cardiovascular Effects. A 56-year-old female gardener, dermally exposed to spilled diazinon of unknown purity, developed sinus tachycardia with no evidence of infarction and showed increased cardiac enzyme (serum glutamate oxalate transaminase, total lactate dehydrogenase creatine phosphokinase) levels. The victim was diagnosed on discharge with acute left ventricular failure (Lee 1989). 

A day after a dose of intravenous methylprednisolone 60 mg a 79-year-old woman developed acute thoracic pain and collapsed. An electrocardiogram showed signs of a myocardial infarction and her cardiac enzyme activities were raised. She died within several hours. Autopsy showed an anterior transmural myocardial infarction and mild atheromatous lesions in the coronary arteries. 

Four women with CREST syndrome or systemic sclerosis had pain and eventually contracture of the masseter muscles during infusion of iloprost for severe attacks of Raynaud s phenomenon (9). The adverse effect was quickly reversed by reducing the infusion rate. There were no electrocardiographic or cardiac enzyme changes. The mechanism of this effect is obscure. 

Cardiac enzyme elevation (creatine kinase-MB, cardiac troponin) may occur on average in 20% to 30% of patients after PCI and is associated with adverse clinical outcomes in the short- and long-term (64), Magnetic resonance imaging... 

Figure 4.12 Analysis of data from Smith and Williamson [188] on inhibition of cardiac enzyme. Measured flux in arbitrary units was obtained from Figures 1 and 2 of [188], A. Flux is plotted as a function inhibitor ATP concentration for [ACCOA]= 16 pM and OAA = 1.13 and 2.25 pM. B. Flux is pi oiled as a function of [ACCOA] at [OAA] = 5 pM at three different concentrations of ATP indicated in figure. C. Flux is plotted as a function of [ACCOA] at [OAA] = 3.1 pM at three different concentrations of SCOA indicated in figure. All data were obtained at pH = 7.4 at 21 °C. Model fits are plotted as solid lines.

Once the heart has stopped fibrillating, the patient is given oxygen via a mask and blood is taken for cell counts, glucose, lipids and cardiac enzymes. Diamorphine (for pain relief) and aspirin are given and, if there are no contraindications, thrombolysis can be started using either streptokinase or tissue plasminogen activator. 

Tests to distinguish between angina and a myocardial infarction involve a full ECG and measurements of specific cardiac enzymes, such as creatine kinase MB and troponin I and T. 

Q4 Cardiac enzymes are released into the blood following heart muscle damage during a heart attack. Creatine kinase, particularly its MB isoenzyme, is one of the most specific of these enzymes, which reaches a peak 24 hours after infarction. It rises and then falls within the first 72 hours of the heart attack. Aspartate transaminase is also released, but levels of this enzyme can be raised in several other conditions, so it is less specific than creatine kinase MB. Troponin T is also specific for myocardial damage and is raised for approximately two weeks following infarction. Finding a high concentration of these enzymes in a patient s blood therefore supports the evidence obtained from the ECG and confirms that the patient has suffered a myocardial infarction. 

After administration of vinorelbine, chest pain occurs in up to 5% of patients. However, subsequent analysis showed that most patients had underlying cardiovascular disease or a tumor in the chest, making interpretation difficult (2,20). Three patients developed acute cardiopulmonary toxicity after vinorelbine therapy (25). The symptoms mimicked acute cardiac ischemia, but with no electrocardiographic changes or raised cardiac enzymes. In two patients, tachypnea, rales, wheezing, and severe dyspnea responded to inhaled salbutamol. One patient developed pulmonary edema and bilateral pleural effusions, which contained no malignant cells when drained. 

Blood arterial pH - decreased (acidosis) [4] Blood bilirubin - increased Blood cardiac enzymes - increased Blood creatinine - increased Blood Hgb/Hct - decreased (anemia)... 

Blood troponin I - increased Blood troponin T - increased Other cardiac enzymes - increased... 

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