Effects of repeated brief episodes of ischemia and reperfusion in isolated perfused rat hearts.

The effects of ischemia and reperfusion on the coronary endothelium and myocardium as well as tolerance to ischemia/reperfusion injury were assessed using isolated retrogradely perfused rat hearts. Repeated brief episodes of myocardial ischemia followed by reperfusion is known to have a protective effect against subsequent myocardial infarction. However, no studies have been performed with perfusion in the absence of blood cells to determine the effect of repeated ischemia and reperfusion on the coronary endothelium and myocardium. Using the Langendorff perfusion technique, rat hearts were subjected to a 30-, 10-, 5-, or 2-min period of low-flow perfusion by reducing the coronary flow to 3 ml/min followed by reperfusion at 20 ml/min for the same period of time. Control perfusion was then performed at a constant flow rate of 20 ml/ min for 60 min. Acetylcholine-induced coronary vasodilation was significantly (P < 0.05) lower in hearts subjected to 30 min of ischemia and 30 min of reperfusion when compared with the control hearts. Myocardial creatinine kinase (CK) activity was significantly reduced (P < 0.01) in hearts subjected to ischemia and reperfusion for either 30, 10, or 5 min. To assess the effect of repeated episodes of ischemia and reperfusion, the following protocols were used: a control study with constant perfusion for 60 min (group A), 30 min of ischemia and 30 min of reperfusion (group B), three 10-min episodes of ischemia and reperfusion (group C), six 5-min episodes of ischemia and reperfusion (group D), and 15 2-min episodes of ischemia and reperfusion (group E). Acetylcholine-induced coronary vasodilation was significantly inhibited in group B (80% +/- 12%, P < 0.05) and group C (70% +/- 13%, P < 0.01), but did not change significantly in either group D (123% +/-19%) or group E (142% +/- 15%), compared with the control group (group A; 127% +/- 15%, mean +/-SEM). Nitroglycerin-induced coronary vasodilation was not altered by ischemia/reperfusion in any group. In contrast, myocardial CK activity was significantly lower in group B (3.6 +/- 0.6IU/mg protein, P < 0.01), group C (3.2 +/- 0.1 IU/mg protein, P < 0.01), and group D (3.3 +/- 0.21U/mg protein, P < 0.01) than in group A (47 +/- 6.7 IU/mg protein). The myocardial CK activity of group E was not significantly different from that of group A, but was significantly higher than in groups B, C, and D (P < 0.01). In isolated perfused rat hearts, both the coronary endothelium and myocardium are damaged by repeated episodes of ischemia and reperfusion. However, the coronary endothelium is more resistant to such damage than is the myocardium.

Mechanism of rethrombosis after thrombolytic therapy: angioscopic findings and investigation of the coagulation system in dogs.

The purpose of this study was to angioscopically observe the process of thrombolysis after intracoronary administration of thrombolytic agents and to investigate the effects of these agents on coagulation/fibrinolysis systems in dogs. The coronary endothelium was removed and thrombus formation was confirmed by angioscopy. In the tissue plasminogen activator (tPA) group (n=8), complete thrombolysis occurred in all animals, but thrombolysis was incomplete in the urokinase (UK) group (n=6). The plasma level of plasmin alpha2-plasmin inhibitor complex peaked at 15 minutes after treatment in both the tPA and UK groups. Plasma thrombin-antithrombin III (TAT) complex decreased transiently at 15 minutes after tPA administration but increased at 30 and 60 minutes (P<0.05). In the UK group, plasma TAT also showed a transient decrease followed by an increase, which was minimal compared with that in the tPA group. Plasma TAT decreased transiently after infusion of tPA and subsequently increased to above the pretreatment level, suggesting a risk of rethrombosis after successful recanalization.

The prevalence and prognostic significance of arrhythmias in Duchenne type muscular dystrophy.

To investigate the prevalence and prognostic significance of cardiac arrhythmias in Duchenne type muscular dystrophy 24-hour ambulatory ECG was performed in 80 patients with Duchenne type muscular dystrophy, and they were followed up for 5 years. Various arrhythmias were observed in 63.8% (51 of 80) of the patients. Ventricular premature beats were found in 30% (24 of 80), and the incidence of ventricular premature beats increased as the clinical severity of skeletal muscle involvement advanced. Forty-seven patients survived for 5 years, but the incidence of arrhythmias increased from 38.3% (18 of 47) to 74.5% (35 of 47) (p < 0.001). During the 5-year period, four of 33 deaths were sudden. Malignant ventricular premature beats (ventricular couplets, ventricular tachycardia, and R-on-T-type ventricular premature beats) were observed in three of these four patients. It appears that cardiac arrhythmias are a common complication of Duchenne type muscular dystrophy and that the incidence of ventricular arrhythmias increases with the progression of myocardial involvement. There is an association between ventricular arrhythmias and sudden death, but the reduction of ventricular arrhythmias may not reduce the incidence of episodes of sudden death.

Oxypurinol limits myocardial infarct size in closed chest dogs without pretreatment.

The authors tested whether allopurinol or oxypurinol could limit infarct size when treatment was started just prior to reperfusion and continued until sacrifice. In closed chest, anesthetized dogs, a branch of the left coronary artery was reversibly occluded for 90 mins followed by 24 h of reperfusion. Fifteen minutes prior to reperfusion, dogs received a bolus of either allopurinol (10 dogs), or oxypurinol (nine dogs), 10 mg/kg intravenously, followed by a 24 h infusion, 55 mg/kg/day. Eleven control dogs received equal volumes of saline. Investigators were blinded to the identity of the agent. Hearts were removed 24 h after reperfusion. Arrhythmias for 30 mins after reperfusion were quantitated. Oxypurinol caused 28% less of the risk zone to infarct for any level of collateral flow than that seen in the controls. This difference was significant. Allopurinol-treated hearts averaged only 18% less infarction and did not achieve significance. Ventricular arrhythmias and mortality did not differ among the three groups. Therefore, unlike allopurinol, oxypurinol with continued administration can limit tetrazolium-indicated necrosis in the dog heart in the absence of pretreatment.

Tetrazolium artifactually indicates superoxide dismutase-induced salvage in reperfused rabbit heart.

We tested the ability of a single dose of superoxide dismutase to induce salvage of reperfused rabbit myocardium. Infarct size was measured by tetrazolium method following 3, 24, or 72 h of reperfusion. In addition, the 24 h reperfused hearts were examined to determine if the drug induced salvage in those hearts was reflected in the histology. A coronary arterial branch was occluded for 45 min and then allowed to reperfuse for 3, 24 or 72 h. At the end of the reperfusion period the hearts were removed, perfusion stained with triphenyl tetrazolium, and fixed in buffered formalin. The hearts were sectioned and infarct size was determined in all groups. In addition, the 24 h heart slices were prepared for histology with H&E staining. The results revealed that 5 mg/kg hSOD treatment was associated with smaller infarcts in the 3 and 24 h groups but that differences were no longer apparent in the 72 h group. The 24 h control hearts showed good correlation between infarct size by TTC and that by conventional histology. In the 24 h treatment hearts, however, infarcts by TTC averaged only about 1/2 the size of those by conventional histology. We conclude that a single dose of hSOD fails to offer a sustained reduction of infarct size. Furthermore, histology from the 24 h reperfused group revealed that hSOD did not delay the onset of necrosis but rather simply caused dead tissue to retain its ability to reduce the tetrazolium salts.

Influence of peripheral intravenous contrast injection on the QRS complex in healthy men.

The influence of acute plasma expansion induced by the administration of sodium containing hyperosmolar contrast medium on Frank lead electrocardiograms was investigated in 10 healthy male volunteers. The major electrocardiographic changes after injection of the contrast medium were a significant decrease in the amplitudes of Rx, Ry, and Qz and the maximal spatial QRS voltage, and a significant increase in the amplitude of Sx. The echocardiographic left ventricular end diastolic dimension tended to be larger after the injection, whereas no significant change occurred in the left ventricular systolic dimension. The electrocardiographic changes in this study were the opposite of those expected with the Brody effect. Although the precise mechanism underlying these findings is unclear, the increased intracardiac blood volume may have caused a decrease in the QRS voltage by a short circuiting effect. Alternatively if the activation in the left ventricle is assumed to be predominantly tangential the QRS voltage should have decreased with the Brody effect. The Brody effect may lead to an erroneous interpretation of electrocardiograms in certain clinical settings.

Electrocardiographic changes due to sauna bathing. Influence of acute reduction in circulating blood volume on body surface potentials with special reference to the Brody effect.

Sauna bathing causes profuse sweating, which could lead to an acute reduction in the circulating blood volume and the intraventricular blood volume. Sauna bathing thus provides a good clinical model with which to evaluate the inter-relation between the body surface potentials and the intraventricular blood mass. After bathing the internal dimension of the left ventricle in diastole was appreciably decreased, whereas the spatial QRS magnitude and the magnitudes of the R and Q waves in lead Z and of the S wave in lead X were significantly increased. These findings indicate that a decrease in the intraventricular volume was accompanied by an increase in the body surface potential and contradict the Brody effect.

[Evaluation of poor R wave progression by cross-sectional echocardiography with wall motion index].

Poor R wave progression (PRWP) in the precordial leads on the electrocardiogram in an often used but ill-defined electrocardiographic finding of antero-septal myocardial infarction. In view of the fact that the cross-sectional echocardiogram (CSE) provides a reliable method for detecting the presence and location of regional asynergy associated with acute myocardial infarction, 47 patients (myocardial infarction; 27, other disease; 20) with PRWP were selected to investigate whether or not CSE could be useful for differentiating the cases showing PRWP with myocardial infarction from those without myocardial infarction. On CSE, the left ventricle was divided into 9 segments, and to grade the severity of segmental asynergy, each segment was assigned a numerical score based upon the type of wall motion. These scores were assigned as follows; hyperkinesis: -1, normal: 0, hypokinesis: +1, akin sis: +2, and dyskinesis: +3 (Heger, 1979). The total wall motion index (WMI) was obtained by summing the scores for each of the 9 segments. And the antero-septal WMI was also obtained by summing the scores for each of the antero-septal segments. The antero-septal WMI in patients with myocardial infarction (4.45 +/- 2.59) was significantly greater than that in patients with other diseases (-0.1 +/- 2.38) (p less than 0.001). The antero-septal WMI equal to or more than +3 was found to be the most useful parameter in identifying the cases with myocardial infarction (sensitivity: 81.5%, specificity: 85.0%). Consequently, it can be concluded that CSE is quite useful for differentiation of PRWP between the cases with or without myocardial infarction.

Sequential changes in high frequency notches on QRS complexes in progressive muscular dystrophy of the Duchenne type--a 3-year follow-up study.

In a 3-year follow-up study, sequential changes in the number of high frequency notches (HFN) on QRS complexes were investigated on 72 cases with progressive muscular dystrophy of the Duchenne type (PMD). The patients were classified into eight stages from the mildest, S(1), to the most severe, S(8), according to Swinyard-Deaver's criteria. The number of HFN progressively increased with advancing Swinyard-Deaver's stage. In the terminal stage, however, the number of HFN tended to decrease. The present observations show that the patient tends to have a small number of HFN in the early stages of the disease; with increasing severity of the disease he develops a larger number; in the terminal stage he again exhibits relatively few notches. It is concluded therefore that significant increases or decreases in the count of HFN on QRS complexes can be useful indicators for estimating the extent and severity of cardiac involvement in PMD.

Primary hemangiopericytoma of the heart. A case report.

Hemangiopericytoma (HP) represents a rare cellular vascular tumor. The present report of primary HP of the heart in a 53-year-old Japanese male is the first of its kind. Most of the tumor masses were removed, but masses tightly adhering to both the pericardium and the epicardium were not excised because of profuse bleeding. The patient has remained free of complaints for 10 months post-operatively. Non-invasive methods including a chest X-ray, echocardiogram, and thallium-201 myocardial imaging were found to be useful adjuncts of the diagnosis of cardiac tumor.

Newly developed systolic murmur in patients with a transvenous pacemaker.

We encountered four cases in which a transvenous cardiac pacemaker produced a systolic musical murmur in the absence of any complications. This systolic murmur appeared only when the pacing was being cut off and disappeared soon after the pacing had been turned on. Although the exact mechanism of production of the murmur remains uncertain, several possible mechanisms for its occurrence are discussed. It is apparent from this study that a systolic murmur can newly occur without any obvious cause in patients with a transvenous pacemaker.