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Early peak creatine kinase activity is not always a marker of successful reperfusion with myocardial salvage in patients with reperfused anterior acute myocardial infarction.

BACKGROUND: Although early peak creatine kinase activity (peak CK) is considered a reliable marker of coronary reperfusion in patients with acute myocardial infarction (AMI), whether early peak CK indicates good myocardial salvage is unclear. Moreover, some patients have late peak CK despite successful reperfusion, and its clinical implication remains to be elucidated. METHODS AND RESULTS: We examined the association of the time to peak CK with predischarge left ventricular function in 124 patients with a first AMI who had successful reperfusion within 6 hours from symptom onset. Patients were classified according to the time from reperfusion to peak CK: group A, 61 patients with peak CK < 6 hours; group B, 42 with peak CK from 6 to 12 hours; and group C, 21 with peak CK > 12 hours. There were no differences among the 3 groups in age, sex, method of reperfusion, time from symptom onset to reperfusion, collateral circulation, or the extent of risk area estimated by number of leads with ST-segment elevation. Left ventricular ejection fraction measured by predischarge left ventriculography was lowest in group A, followed by group B, and highest in group C (median values, 43%, 52%, and 60%, P < .01). Left ventricular dysfunction (left ventricular ejection fraction < or = 40%) occurred in 26 (43%) patients in group A, 8 (19%) in group B, and none in group C (P < .01). CONCLUSIONS: We conclude that compared with early peak CK, late peak CK consistently reflects good myocardial salvage in patients with anterior AMI who had successful reperfusion within 6 hours from symptom onset.

Adult↗

A single dose of milrinone facilitates separation from cardiopulmonary bypass in patients with pre-existing left ventricular dysfunction.

Milrinone is used during cardiac surgery to facilitate separation from cardiopulmonary bypass (CPB) and/or to treat myocardial dysfunction in the post-bypass period. We have demonstrated, in patients with preoperative depression of systolic function undergoing aorto-coronary artery bypass surgery, sustained improvement in cardiac function after a single loading dose of milrinone 50 micrograms kg-1, administered at the end of bypass, thus significantly decreasing the need for beta-agonist therapy.

Adult↗

Pre-thrombotic state and impaired fibrinolytic potential in coronary heart disease patients with left ventricular dysfunction.

Patients with coronary heart disease (CHD) are at considerable risk for recurrent ischaemic events. A pre-thrombotic state and/or impaired fibrinolysis might play an important role in causing recurrent ischaemic events. Two hundred and fifty-seven CHD patients underwent the dobutamine stress echocardiography test (DSE) to investigate the possible presence of inducible ischaemia; 89 patients showed evidence of stunned and/or necrotic myocardium (resting wall motion abnormalities). Factor VIII activity and fibrinogen levels were significantly higher in patients with stunned/necrotic myocardium than in CHD patients with normal resting wall motions (factor VIII activity, P = 0.004; fibrinogen, P = 0.04). Of interest, after stimulating the fibrinolytic system with the DSE test, plasminogen activator inhibitor-1 activity was significantly higher in patients with necrotic/stunned myocardium than in patients with resting normal wall motion (P = 0.03), whereas tissue-type plasminogen activator activity after the DSE test was significantly lower in patients with stunned/necrotic myocardium than in patients with normal wall motion (P = 0.001). Overall, 30 CHD patients developed induced ischaemia (new wall motion abnormalities) during the DSE test. CHD patients with stunned and/or necrotic myocardium presented decreased fibrinolytic potential and the presence of a hypercoagulable state due to increased factor VIII activity, and fibrinogen levels. Therefore, these CHD patients must be considered at high risk of re-developing coronary thrombosis and might benefit from a more aggressive anticoagulant therapy.

Aged↗

Arginine vasopressin V1-receptor antagonism in an ovine model of acute myocardial infarction.

Arginine vasopressin (AVP) has an uncertain role in the pathogenesis of increased myocardial and other regional vascular resistance after cardiac injury. The extreme increase in plasma AVP levels observed in some individuals after myocardial infarction potentially exacerbates already compromised myocardial perfusion. We assessed whether blockade of AVP, by administration of the specific V1-receptor antagonist OPC-21268, can reduce the severity of myocardial injury after embolization in our ovine model of acute myocardial infarction. Embolizations resulted in a pattern of changes in ECG and cardiac enzymes consistent with moderate to severe acute myocardial infarction, resulting in left ventricular dysfunction [left ventricular ejection fraction (LVEF) reduced from 52-53% to 38%]. However, no statistically significant differences were observed between groups in hemodynamic or neurohumoral indices of myocardial damage. By contrast, the hypothalamus-pituitary-adrenal (HPA) response [including plasma AVP (p < 0.01), adrenocorticotropic hormone (ACTH; p < 0.01), and cortisol (p < 0.01)) to embolizations was significantly increased in the sheep infused with OPC-21268. In conclusion, whereas plasma HPA responses differed between the two groups, the similar responses in cardiac enzymes, LVEF, and hemodynamic and neurohumoral factors in both groups does not support a role of V1 receptor-mediated exacerbation of myocardial injury in this model of myocardial infarction. Assessment of different receptor antagonists or examination of other models of cardiac injury may further clarify the role of the markedly increased AVP levels that can occur in myocardial infarction.

Adrenocorticotropic Hormone↗