Circulation
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Modest survival benefits have been reported in patients with acute myocardial infarction complicated by cardiogenic shock who were treated with early surgical revascularization or thrombolytic therapy. To determine whether coronary angioplasty improves survival, 87 patients with cardiogenic shock complicating acute myocardial infarction at the University of Michigan, Ann Arbor, Michigan, from 1975 to 1985 were retrospectively analyzed. Patients in group 1 (n = 59) were treated with conventional therapy; patients in group 2 (n = 24) were treated with conventional therapy and angioplasty. ⋯ The 30-day survival was significantly improved for group 2 patients (50% vs. 17%, p = 0.006). Survival in group 2 patients with successful angioplasty was 77% (10 of 13 patients) versus 18% (two of 11 patients) in patients with unsuccessful angioplasty, (p = 0.006). The findings suggest that angioplasty improves survival in cardiogenic shock compared with conventional therapy with survival contingent upon successful reperfusion of the infarct-related artery.
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Ventricular-assist devices (VAD) have increased survival in patients with postcardiotomy shock, but the predictors of success need to be elucidated. We evaluated 45 patients treated with centrifugal (n = 18) or pulsatile (n = 27) VAD for postcardiotomy cardiogenic shock to determine the effect of perioperative myocardial infarction (PMI) on survival. The patients ranged in age from 15 to 72 years (mean age, 55.1 years). ⋯ Definite PMI was much more common in nonsurvivors (72.7%) than in survivors (8.3%) (p less than 0.05). However, Group 2 nonsurvivors were weaned despite PMI in 100% of cases. These data suggest that, although PMI is a strong negative determinant of survival in postcardiotomy patients, it cannot be considered a contraindication because it does not preclude myocardial recovery.
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Arginine vasopressin is elevated in congestive heart failure. To determine the effect of arginine vasopressin upon systemic hemodynamics and regional blood flows, we administered the specific inhibitor of the vascular action of vasopressin [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)-tyrosine]-arginine vasopressin [d(CH2)5Tyr(Me)AVP] to 15 dogs with chronic right-heart failure produced by tricuspid avulsion and progressive pulmonary artery constriction. The animals exhibited increased plasma arginine vasopressin and norepinephrine levels. ⋯ Pretreatment also led to a decrease in mean aortic pressure after vasopressor inhibition. In contrast, administration of d(CH)2)5Tyr(Me)AVP to 11 sham-operated animals or administration of normal saline to nine sham-operated and eight heart-failure dogs was without effect either in the absence or in the presence of adrenergic receptor blockade. Thus, arginine vasopressin participates in the control of the circulation in right-sided congestive heart failure, with both a direct constrictor action on blood vessels and an indirect action by inhibition of the sympathetic nervous system.
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Left ventricular end-systolic pressure-wall thickness and pressure-segment length relations have been used to assess regional myocardial contractility. The purpose of these studies was to determine whether the method of afterload alteration, coronary perfusion pressure, and the definition of end systole affected regional end-systolic relations. In paced open-chest pig hearts (n = 10), left ventricular pressure, wall thickness, and segment length were measured during vena caval occlusions. ⋯ A decrease in the coronary perfusion pressure, particularly with ischemia, shifted the x-axis intercepts of both Emax and Ees in a direction consistent with a decrease in contractility. Thus, regional end-systolic relations in intact hearts are dependent on the method of afterload alteration and the coronary perfusion pressure. Furthermore, Emax differs from Ees, so the assessment of regional relations depends on how end systole is defined.
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The aim of this study was to differentiate myocardial reperfusion injury from that of ischemia. We assessed the role of the myocardial adenosine 5'-triphosphate (ATP) catabolites, hypoxanthine and xanthine, generated during ischemia and the early phase of reperfusion, in reperfusion injury by modulating adenosine transport and metabolism with specific metabolic inhibitors. This was followed by intracoronary infusion of exogenous hypoxanthine and xanthine. ⋯ Left ventricular performance in Group 1 decreased from 76.8 +/- 7.6 to 42.9 +/- 9.8 and 52.3 +/- 8.4 dynes/cm2 x 10(3) (p less than 0.05), while myocardial ATP decreased from 30.9 +/- 2.2 to 17.2 +/- 1.0 and 16.5 +/- 1.0 nmol/mg protein during 30 and 60 minutes of reperfusion, respectively (p less than 0.05 vs. preischemia). Ventricular function in Group 2 dogs completely recovered within 30 minutes of reperfusion, and myocardial ATP recovered to the preischemic level at 60 minutes of reperfusion. In Group 3, left ventricular performance was depressed by 39% and 30% during 30 and 60 minutes of reperfusion (p less than 0.05), respectively, and myocardial ATP did not recover during reperfusion despite a significant intramyocardial adenosine accumulation.(ABSTRACT TRUNCATED AT 400 WORDS)