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The validity of angiographic collateral grade according to the Rentrop classification during acute myocardial infarction (AMI) and its relation to flow in occluded coronary arteries before angioplasty have never been evaluated.We assessed the validity of the angiographic collateral grade according to Rentrop classification in relation to collateral pressure and flow beyond occluded coronary arteries during AMI. Pressure distal to coronary artery occlusions before balloon dilatation was measured in 111 patients undergoing angioplasty for AMI. We calculated the collateral flow index (CFI) and compared it to observed Rentrop grade and measured creatine kinase sum.The values of pressure distal to coronary artery occlusions with respect to collateral grades 0 to 3 were 33 +/- 12, 37 +/- 13, 42 +/- 10, and 60 +/- 14 mm Hg (P.0001). Overall CFI was 0.35 +/- 0.13 (median 0.33), with CFI values of 0.3 +/- 0.13, 0.33 +/- 0.13, 0.39 +/- 0.1, and 0.57 +/- 0.2 for collateral grades 0 to 3, respectively (P.0001). Larger creatine kinase elevation (P.016) and higher white blood cell count (P.022) were recorded in the lowest tertile CFI compared with highest tertile CFI group; but no difference in the global, regional, or infarct-related regional left ventricular contraction was found.These observations demonstrate that the Rentrop classification is valid in AMI patients with occluded coronary arteries and that collaterals are recruited acutely. These collaterals, whose pressure-derived CFI during AMI was shown for the first time to be higher than its value reported in chronic conditions, may limit the immediate myocardial damage or the systemic inflammatory response. No impact on global or regional cardiac contraction was detected in a population where most patients were treated early.

This study was performed to examine the hypothesis that an early attenuation of nitrate effect caused by nitrate tolerance can be overcome by dose increase. We compared hemodynamic effects of constant dose (40 to 120 mg) of oral isosorbide dinitrate (ISDN) given every 6 hours for three doses followed by 12 hours of nitrate washout interval with those of escalating dose (40 mg, 80 mg, and 120 mg) in two similar groups of patients with chronic congestive heart failure. Escalating ISDN dose resulted in a progressive increase in ISDN blood level and overcame early attenuation of effect occurring with a constant dose. At peak effect of the third ISDN dose, a significantly greater reduction was seen in mean right atrial pressure (-59% +/- 27% vs -20% +/- 22%, p0.01), mean pulmonary artery pressure (-29% +/- 11% vs -11% +/- 15%, p0.01) and mean pulmonary artery wedge pressure (-39% +/- 19% vs -19% +/- 23%, p0.05) with the escalating dose. These findings demonstrate that early attenuation of hemodynamic effect caused by nitrate tolerance can be overcome by dose escalation.

Both arteriolar vasodilation with hydralazine and venodilation with nitroglycerin have been shown to favorably alter the hemodynamic profile in patients with chronic mitral regurgitation. Since these therapeutic modalities exert their effects by different mechanisms, this study was designed to assess hemodynamic response to both drugs given individually and in combination at rest and during isometric exercise in patients with chronic mitral regurgitation of various etiologies. When used individually, hydralazine caused larger increase in heart rate, cardiac index, stroke volume index, and systemic vascular resistance both at rest and during exercise. In contrast, nitroglycerin administration was associated with a superior effect on mean pulmonary artery pressure and V wave amplitude at rest and on mean right atrial and mean pulmonary artery wedge pressures at rest and during isometric exercise. In comparison with hydralazine alone, combination therapy enhanced the reduction in right atrial pressure (4 +/- 1 versus 0 +/- 2 mm Hg, p < 0.05), mean pulmonary arterial pressure (11 +/- 5 versus 1 +/- 3 mm Hg, p < 0.05), and the V wave amplitude (15 +/- 6 versus -5 +/- 3 mm Hg, p < 0.05) at rest and resulted in a larger reduction in exercise values of mean pulmonary artery pressure (-11 +/- 7 versus -3 +/- 5 mm Hg, p < 0.05) and mean pulmonary arterial wedge pressure (-11 +/- 5 versus -5 +/- 3 mm Hg, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

In acute coronary syndromes (ACSs), blood transfusion (BT) has been associated with worse outcomes. The impact of BT among patients with acute decompensated heart failure (ADHF) remains unknown.Propensity score analysis of patients with ADHF with and without BT in a national heart failure (HF) survey was used in this study.Of the 4,102 enrolled patients, 2,335 had ADHF, of whom 166 (7.1%) received BT. These patients were older (75.6% vs 73.6%, P = .04), more likely to be females (54.8% vs 43.9%, P = .007), more likely to have diabetes (59.0% vs 51.1%, P = .04) and renal dysfunction (59.0% vs 40.2%, P.001), and more likely to receive inotropes (16.9% vs 8.0%, P.001), but they had similar rates of ACS (41.0% vs 39.4%, P = .69) and prior HF (64.5% vs 70.0%, P = .23). Nadir hemoglobin levels were commonly10 g/dL in BT patients (92.7% vs 8.0%); 15 BT patients had bleeding complications, of which 10 are major bleeding. Major predictors for BT were ACS (OR 1.85, 95% CI 1.15-2.96), inotropes use (OR 2.36, 95% CI 1.22-4.55), and nadir hemoglobin (OR 0.18 per 1 g/dL increase, 95% CI 0.14-0.22). In-hospital, 30-day, 1-year, and 4-year unadjusted mortality rates were higher for BT patients (10.8% vs 5.2%, P = .02; 11.0% vs 8.5%, P = .27; 39.6% vs 28.5%, P = .03; 69.5% vs 59.5%, P = .01, respectively). However, in 103 propensity-matched pairs (c-statistic 0.97), short-term mortality tended to be lower with BT (8.7% vs 14.6%, P = .20; 9.7% vs 18.4%, P = .08; 38.8% vs 42.7%, P = .59; and 72.8% vs 76.7%, P = .52, respectively).Acute decompensated HF patients receiving BT had worse clinical features and unadjusted outcomes, but BT per se seemed to be safe and perhaps even beneficial.

Patients presenting with ST-elevation myocardial infarction (STEMI), whose symptoms and electrocardiographic changes completely resolve upon admission and before the administration of reperfusion therapy, pose a therapeutic dilemma. The optimal management of this syndrome, termed here as transient STEMI (TSTEMI), has not yet been fully determined. We describe 69 prospectively recorded patients with TSTEMI, of which 63 patients (56.7 +/- 11 years, 48 men) were available for long-term follow-up out of 1244 consecutive patients with acute myocardial infarction (5%). Patients with TSTEMI treated with intravenous isosorbide dinitrate, aspirin, and clopidogrel, and/or with glycoprotein IIb/IIIa inhibitors were compared with a control group of matched patients with STEMI without resolution, who were treated conventionally. The time interval from symptom onset to presentation at the emergency department of patients with TSTEMI was 1.7 +/- 1.3 hours, and to first recording of ST elevations, 1.5 +/- 1.4 hours. Symptoms and electrocardiographic changes fully resolved 1.2 +/- 0.8 hours later, 1 hour after aspirin and nitrate administration. Coronary angiography, performed 36 +/- 39 hours (median, 24 hours) from admission, demonstrated no obstructive lesion or single-vessel obstructive disease in 43 patients (70%). Primary coronary intervention was performed in 48 patients (77%), and 8 patients (13%) were referred to surgery. Left ventricular ejection fraction was within normal limits, and peak creatine kinase was mildly elevated. Patients with TSTEMI had less extensive coronary artery disease (P.038), better thrombolysis in myocardial infarction flow on angiography (P.01), lower peak creatine kinase level (P.001), higher left ventricular ejection fraction (P.0001), and lower likelihood to sustain a second additional coronary event after index admission (P = .024) than patients with STEMI. Transient STEMI was associated with less myocardial damage, less extensive coronary artery disease, higher thrombolysis in myocardial infarction flow grade in culprit artery, and better cardiac function. These data suggest that immediate intense medical therapy with an early invasive approach is an appropriate therapy in patients with TSTEMI.

Background Patients with recurrent acute myocardial infarction (AMI) are at increased risk for morbidity and mortality. We compared the outcome of patients with recurrent AMI hospitalized in coronary care units in the prereperfusion and reperfusion eras. Methods The study population comprised 2 large-scale cohorts with recurrent AMI: (1) 1415 (24%) of 5839 consecutive patients with AMI hospitalized in 1981 to 1983 (Secondary Prevention Reinfarction Israeli Nifedipine Trial [SPRINT] Registry) and (2) 1093 (25%) of 4317 patients with AMI from three national surveys performed in 1992 to 1996. Results Patients in the 1990s had significantly lower rates of heart failure and cardiogenic shock. The 7-day mortality declined from 18% in 1981-1983 to 10% in 1992-1996 (adjusted odds ratio [OR] 0.57 [0.44-0.75]), the 30-day mortality rate from 26% to 16% (OR 0.56 [0.44-0.71]), and the 1-year mortality rate from 39% to 26% (adjusted hazard ratio [HR] 0.64 [0.54-0.75]), respectively. In the 1992-1996 cohort, the adjusted risk of 7-day, 30-day, and 1-year mortality for patients with recurrent AMI treated with thrombolysis in comparison to patients without thrombolysis was OR 1.69 (1.07-2.65), 1.51 (1.03-2.23), and HR 1.18 (0.90-1.55), respectively. The mortality rate among patients treated with early percutaneous transluminal coronary angioplasty/coronary artery bypass grafting was 3% versus 12% at 7 days (OR 0.36 [0.16-0.73]), 7% versus 18% at 30 days (OR 0.45 [0.25-0.77]), and 16% versus 29% at 1 year (HR 0.64 [0.46-0.96]), in comparison to patients without revascularization. Conclusion The prognosis of patients with recurrent AMI improved significantly during the reperfusion era. Although thrombolysis may have a limited therapeutic effect among patients with recurrent AMI, an interventional approach seems more appropriate when indicated. A randomized trial of thrombolysis versus early revascularization is needed in patients with recurrent AMI. (Am Heart J 2001;141:478-84.)