Heart and vessels. Supplement最新文献

Twenty thoroughbred race horses were selected for postmortem cardiopathological study of sudden cardiac death; ten of the twenty horses died suddenly. In order to define accurately the morphological changes observed in these ten hearts, ten other thoroughbred race horses considered to have normal hearts were selected as a control group and studied by postmortem coronary angiography. Of the ten horses that died suddenly, eight were witnessed to have died either during or shortly after training or racing. The death was instantaneous except in one horse, which showed ventricular tachycardia and died 4.5 h after a race. The other two died unexpectedly in the stable at night. Pathologically, the horses that died suddenly generally showed multifocal myocardial lesions that were ischemic and fibrotic. These lesions were found in the atrial tissue close to the sinoatrial (SA) node and in the atrioventricular (AV) junction, including the upper portion of the interventricular septum. Such myocardial lesions were often associated with vascular changes including arterio- and/or arteriolosclerosis. Angiographically, the SA node appeared to be perfused by atrial branches of the left and right coronary arteries. One branch originating from the left coronary artery gave off a few branches into the AV junction. These pathological findings, mainly consisting of both atrial lesions and lesions in the AV junction, were similar to those observed in horses with either atrial fibrillation, SA block, or paroxysmal ventricular tachycardia. A finding of particular interest was the angiographic demonstration that the blood supply to the AV junction partly came from the SA node artery.(ABSTRACT TRUNCATED AT 250 WORDS)

To investigate the long-term course or natural history of Romano-Ward syndrome, 131 cases from the affected side of 13 families with the syndrome were examined by electrocardiography and a review of the histories. The patients were followed up for 2-13 years, with an average of 7.2 years. Five patients (3.8%) died suddenly, four with QT prolongation and one with a normal QT interval. Fourteen patients (10.7%) with QT prolongation developed episodes of syncope, whereas 58 patients (44.3%) showed only QT prolongation without syncopal episode. Three of the thirteen families were asymptomatic, with no cases of syncopal episodes or sudden death, although more than 50% of the examined cases in these families showed definite QT prolongation. In the other ten families, syncopal attacks and/or sudden death occurred in some of the family members. In two of the ten symptomatic families, the probands developed their first syncopal attacks very late in their lives (at the ages of 64 and 75 years), and both families had been asymptomatic before these elder family members became symptomatic. In two cases, syncopal attacks disappeared after electrocardiographic improvement. The present study suggests that: (a) asymptomatic families of Romano-Ward syndrome exist, (b) asymptomatic families may sometimes become symptomatic, and (c) regression of the manifestations of Romano-Ward syndrome may occur in some cases.

We tested the multiple-wavelet hypothesis by studying the initiation and maintenance of atrial fibrillation in normal mules, horses, cows, calves, and goats. Persistence of atrial fibrillation in animals with a large atrial mass was compared with results in adult goats and calves having a smaller atrial mass. Atrial stimulation in clinically normal cows, mules, calves, and goats was accomplished using an intra-atrial stimulating catheter with rapid atrial pacing (30/s). Once initiated, atrial fibrillation persisted for 95,120,125 min, 3 days, and 8 weeks in five adult cows, respectively. In contrast, in five calves, atrial fibrillation failed to persist for more than a few minutes. Similar results were found in the small atria of adult goats, indicating that atrial size rather than maturity of the atrial myocardium was responsible. In addition, to demonstrate that this was not a species-dependent phenomenon, it was shown in adult mules that atrial fibrillation could persist for 24 h or more once initiated. These studies are consistent with the multiple-wavelet hypothesis for initiation and maintenance of atrial fibrillation. We also studied the ventricular response in atrial fibrillation. We found that as many as nine consecutive atrial responses can be concealed within the atrioventricular (AV) node associated with a long R-R interval during atrial fibrillation. Although concealment of rapid atrial activity normally occurred in the AV node, one case of infranodal block was observed. It has also been suggested that subsidiary AV junctional pacemakers may be the cause of the ventricular irregularity. However, our experimental studies using microelectrodes in isolated tissue and extracellular bundle of His recordings in intact animals failed to demonstrate that this mechanism was responsible for the irregularity of the ventricular response in atrial fibrillation.

Atrial fibrillation is one of the most common cardiac arrhythmias in humans. It also occurs quite frequently in dogs and horses. Comparative study of this arrhythmia may contribute to better understanding of the pathophysiological mechanisms involved. In this study, we present a quantitative analysis of atrial fibrillation in humans, dogs, horses, and in a kangaroo, making use of histograms and serial autocorrelograms of the ventricular rhythm with and without digitalis medication. Increase in the size of the animal and thus in the size of the heart is accompanied by a decrease in ventricular rate. The ventricular rhythm was random in the dog, kangaroo, and man, but periodicity was present in the horse. Digitalis decreased the ventricular rate in all species studied and enforced the periodicity in the horse. The differences in the atrial excitation process, atrioventricular (AV) conduction, and ventricular behavior between the four species studied are small when compared with the differences in their heart size. We conclude that in evolution, as far as the heart is concerned, cell size and morphology probably prevail over cell-function.

Atrial fibrillation (AF) is the most frequently observed arrhythmia in milking cows. About 50% of AF-affected cows have a history of ketosis, suggesting a relationship between AF and ketosis. Clinical signs of AF include a sudden decrease in milk production and an unstable appetite. Oral administration of quinidine is effective in the treatment of AF. AF in the pig has been observed only in one breeding animal. The clinical signs included anorexia and abnormal heart sounds. The AF was successfully terminated by the administration of 10 mg/kg quinidine every 8 h. AF in dogs and cats appears as a sign of cardiac failure, although AF may also be observed in large dogs without any underlying cardiac disease. Direct current defibrillation is effective in the treatment of these animals.

The clinical significance of atrial fibrillation was analyzed in cases with chronic or acute heart disease and its significance at the acute and chronic stages of the disease was investigated in various disease groups. The types of disease, number of patients, and incidence of atrial fibrillation were: atrial septal defect (92, 14.1%), mitral valve disease (128, 79.7%), nonrheumatic valvular disease (32, 56.2%), aortic regurgitation (71, 2.8%), aortic stenosis (10, 10.0%), hypertrophic cardiomyopathy (181, 11.6%), dilated cardiomyopathy (111, 37.8%), acute myocardial infarction (823, 9.0%), healthy subjects (31,886, 0.3%). A histopathological and electron-microscopic evaluation of the atrial heart muscle revealed that the advancement of the morphological changes was closely related to the occurrence of atrial fibrillation. Decrease in size of F waves in the electrocardiogram correlated well with the extent of right and left atrial fibrosis. Also, it was noteworthy that the atrial fibrillation in cases with dissecting aneurysm (n = 60) was an expression of the myocardial damage due to the infiltration of the bleeding into the right atrium. Intra-atrial electrogram in 48 patients with various heart diseases revealed that the electric potentials obtained from various parts of the atrium varied to a great extent and finally the patient's condition transformed to that of atrial standstill. We conclude that atrial fibrillation is an expression of some important aspect of the progression of heart disease and is not directly associated with hemodynamic overloading to the atrium. A strategy for quinidine treatment was also introduced.