Left ventricular outflow obstruction induced by tamponade in hypertrophic cardiomyopathy.

Echocardiographic abnormalities of valvular movement described in patients with pericardial effusions have included systolic anterior motion (SAM) of the mitral valve. Published illustrations have shown, however, "pseudo-SAM" rather than true SAM. We report a patient with asymmetric septal hypertrophy whose echocardiogram during tamponade showed true SAM, which was no longer apparent and could not be provoked following resolution of tamponade. Two prior cardiac catheterizations revealed no intraventricular pressure gradients in either normal or postextrasystolic beats. Tamponade was the only stimulus that provoked signs of obstruction in this patient with asymmetric septal hypertrophy.

Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion.

Components of the complement system are known to play an important role in the cytolytic process and in chemotaxis of leukocytes. Cobra venom factor specifically cleaves C3 activity via activation of the alternative (properdin) complement pathway. It does not act directly on C3. If C3 is involved in tissue necrosis after ischemic injury, cobra venom factor might reduce tissue damage after acute coronary occlusion. Accordingly, in 14 control dogs occlusion of the left anterior descending artery was carried out for 24 h. Epicardial electrograms were recorded 15 min after occlusion, and 24 h later transmural specimens for creatine phosphokinase activity (CPK) and for histological analysis were obtained from the same sites. In another 14 experimental dogs, 20 U/kg cobra venom factor was given intravenously 30 min after occlusion. Serum complement levels fell within 2-4 h to <20% of normal. In the control dogs, the relationship between ST-segment elevation and CPK activity 24 h later was: log CPK = -0.06 ST + 1.48 (n = 111 specimens, 14 dogs, r = 0.77). In the experimental dogs, log CPK = -0.024 ST + 1.46 (n = 111 specimens, 14 dogs, r = 0.60), showing significantly different slopes (P < 0.001), i.e., less CPK depression for any level of ST-segment elevation. Histologically, 69 of 71 sites (97%) with ST-segment elevation exceeding 2 mV in the control dogs showed signs of necrosis 24 h later, whereas in the experimental group only 43 of 79 sites (54%) with abnormal ST-segment elevations showed signs of necrosis (P < 0.0005). At the same time, it was shown that the administration of cobra venom factor did not alter cardiac performance, collateral blood flow to the ischemic myocardium or the clotting system, but infiltration of polymorphonuclear leukocytes into the myocardium was decreased. It is concluded that cobra venom factor, by reducing the amount of C3 and C5 substrate available for chemotactic factor generation, or other as yet undefined mechanisms, protects the ischemic myocardium from undergoing necrosis, as judged by histology and local CPK activity. Hence, a new approach to limiting the extent of myocardial infarcts after experimental coronary occlusion, based upon inhibition of complement-dependent inflammatory processes, is demonstrated.

Mechanical circulatory support in postoperative cardiogenic shock.

A 38-year-old white woman had cardiogenic shock after elective mitral valve replacement and was unresponsive to pressor drugs and intra-aortic balloon counterpulsation. A left ventricular assist device (left ventricle to ascending aorta) was implanted 16 hours after the initial operation and provided circulatory support for 8 days. Improvement in the patient's own cardiac performance was documented, and there were no complications attributable to the assist device. However, intercurrent medical problems resulted in clinical deterioration on the fifth day after operation, and the patient died 8 days after operation. The findings in this patient suggest a potential role for this left ventricular assist device in future cases of acute, intractable, but potentially reversible myocardial failure.

Favorable effects of hyaluronidase on electrocardiographic evidence of necrosis in patients with acute myocardial infarction.

To evaluate hyaluronidase's effect in reducing post-infarction myocardial necrosis, we randomized 91 patients with anterior infarction to control (45) or to hyaluronidase-treatment (46) groups. A 35-lead precordial electrocardiogram was recorded on admission and seven days later. Hyaluronidase was administered intravenously after the first electrocardiogram and every six hours for 48 hours. QRS-complex changes were analyzed to assess the drug's effect. Precordial sites with ST-segment elevation (larger than or equal to 0.15 mV) on the initial electrocardiogram that retained an R wave were considered vulnerable for the development of electrocardiographic signs of necrosis. The sum of R-wave voltages of vulnerable sites fell more in the control group than in the hyaluronidase group (70.9 +/- 3.6 per cent [+/- 1 S.E.M.] vs 54.2 +/- 5.0 per cent P less than 0.01). Q waves appeared in 59.3 +/- 4.9 per cent of the vulnerable sites in control versus 46.4 +/- 4.9 per cent in hyaluronidase-treated patients (P less than 0.05). Thus, hyaluronidase reduced the frequency of electrocardiographic signs of myocardial necrosis.

Use of changes in the epicardial QRS complex to assess interventions which modify the extent of myocardial necrosis following coronary artery occlusion.

The goal of this study was to determine if changes in the epicardial QRS complex after coronary artery occlusion (CAO) can be used to evaluate the efficacy of interventions designed to limit infarct size. Forty-one open-chest dogs with CAO were studied: 15 were controls, 18 received hyaluronidase and eight received propranolol starting 20 minutes after CAO. Epicardial ECGs were recorded at specific time intervals to analyze ST-segment elevation and changes in Q and R waves. Transmural specimens were obtained 24 hours after CAO from the same sites at which ECGs were recorded. Q wave development (deltaQ), R wave fall (deltaR), and their combination (deltaR + deltaQ) at 24 hours correlated with the extent of necrosis, as determined by myocardial creatine phosphokinase activity depression and histologic appearance. In the control group ST-segment elevation 15 minutes after CAO (ST15M) predicted changes in Q and R waves 24 hours later; in the treated groups, the same ST15M prior to drug administration resulted in significantly less QRS changes. Thus, 1) Q wave development and R wave fall 24 hours after CAO accurately reflect myocardial necrosis. 2) ST15M predicts subsequent changes in Q and R waves. 3) The efficacy of hyaluronidase and propranolol, agents previously shown to reduce myocardial necrosis, can be detected by less Q wave development and a smaller fall in R wave voltage.

Reduction of infarct size by oxygen inhalation following acute coronary occlusion.

This study was carried out in order to determine the effects of the inspiration of O2-enriched air on the size of myocardial infarction. In 15 anesthetized dogs, epicardial electrograms were recorded from 10 to 14 sites on the anterior surface of the left ventricle before and after intermittent occlusion of the left anterior descending coronary artery or one of its major branches. In each dog, one occlusion was carried out while the fraction of inspired oxygen (FIO2) was 0.20 and the other while the FIO2 was 0.40. With an FIO2 of 0.20 the average ST-segment elevation (ST) was 4.0 +/- 0.6 mV (SEM) and the number of sites exhibiting ST-segment elevations exceeding 2 mV (NST) 15 minutes following occlusion was 6.2 +/- 0.7 sites; comparable values following occlusion with an FIO2 of 0.40 were 1.8 +/- 0.4 mV (P less than 0.01) and 2.7 +/- 0.7 sites (P less than 0;01), reflecting reduction in acute myocardial ischemic injury; An FIO2 of 1.0 did not decrease myocardial injury further. In 24 other dogs, occlusion was maintained for 24 hours. In nine dogs in which FIO2 was increased from 0.20 to 0.40 30 minutes after occlusion, myocardial creatine phosphokinase activity (CPK) was less depressed in sites having comparable levels of ST-segment elevation at 15 minutes than in dogs that respired an FIO2 of 0.20 during the entire 24 hours. All (54) sites with ST-segment elevations greater than 3 mV in the 0.20 FIO2 group showed early signs of myocardial infarction, while only 49% of such specimens showed infarction in the 0.40 FIO2 group. Thus it is concluded that 0.40 FIO2 following an experimental coronary artery occusion decreases acute ischemic injury and reduces the eventual development of necrosis, as evaluated by enzymatic and histological techniques.

Effects of hypoxemia on the extent of myocardial necrosis after experimental coronary occlusion.

Arterial oxygen tension is variable in patients with acute myocardial infarction, and the effect of hypoxemia on the extent of myocardial necrosis after coronary occlusion has not been defined. In 11 anesthetized open chest dogs the left anterior descending coronary artery or one of its major branches was occluded for 20 minutes, and 10 to 15 epicardial electrocardiographic leads were recorded in the distribution and vicinity of the site of occlusion. Average S-T segment elevation and the number of sites showing S-T segment elevation greater than 2 mv, 15 minutes after occlusion were used as indexes of the severity and extent of ischemic injury. After occlusion with an inspired oxygen concentration of 20 percent these indexes were, respectively, 2.0 plus or minus 0.5 mv (mean plus or minus standard error) and 3.6 plus or minus 0.8 sites; the respective values increased to 3.3 plus or minus 0.5 mv (P smaller than 0.01) and 6.7 plus or minus 0.7 sites (P smaller than 0.01) after occlusion with an inspired oxygen concentration of 10 percent, and arterial partial pressure of oxygen decreased from 92 plus or minus 5 to 45 plus or minus 3 mm Hg. In 23 dogs the occlusion was maintained for 24 hours and the S-T segment elevation 15 minutes after occlusion was compared with myocardial creatine phosphokinase (CPK) activity and histologic appearance 24 hours later. In control dogs (inspired oxygen concentration of 20 percent) sites with no S-T segment elevation 15 minutes after occlusion showed normal myocardial CPK activity 24 hours later, whereas in sites with S-T segment elevation exceeding 2 mv there was an inverse relation between S-T segment elevation in each site and its myocardial CPK activity 24 hours later. Histologic examination revealed early myocardial necrosis in 98 percent (82 of 84) of sites with S-T segment elevation greater than 2 mv. In experimental dogs (inhaling a 10 percent oxygen concentration for the first 8 of the 24 hours of occlusion) many sites that showed no S-T segment elevation before hypoxemia was induced exhibited S-T segment elevation before hypoxemia was induced exhibited S-T segment elevations 30 minutes later and showed abnormally low CPK activity and histologic evidence of early necrosis. We conclude that after experimental coronary occlusion, hypoxemia is deleterious because it substantially increases myocardial damage.