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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ambulatory 24 hour electrocardiographic monitoring was performed in 124 patients before cardiac catheterization and coronary angiography. Ventricular premature beats were demonstrated in 83% of all patients. Ectopic activity persisted for at least 3 of the 24 hours in 75% of the 84 patients with coronary heart disease, 61% of 28 with other heart disease and in 24% of 12 normal subjects. The prevalence and grade of ventricular premature beats were increased in the 57 patients with multivessel disease compared with values in the 27 patients with one vessel disease (P less than 0.01). Findings in the latter group did not differ from those of normal subjects. The presence of elevated left ventricular end-diastolic pressure of asynergy was associated with increased ventricular ectopy. Of 15 patients having both asynergy and elevated left ventricular end=diastolic pressure (more than 19 mm Hg), 40% had paroxysms of ventricular tachycardia and 67% had coupled beats; these findings were present in 6 and 12%, respectively, of the 34 patients without asynergy or pressure abnormality (P less than 0.005). Repeat monitoring performed in 65 patients demonstrated greater reproducibility of advanced grades of ventricular premature beats among those with the most severe lesions. For the individual patient the prevalence and grade of ventricular ectopy may not always correlate with the severity of coronary artery disease or degree of left ventricular dysfunction.
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PMID:Ventricular premature beats and anatomically defined coronary heart disease. 6 91

Eleven patients with short P-R intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A-H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P-R and A-H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an exprerssion of the "enhanced A-V conduction" that had been manifested in sinus beats by short P-R and A-H intervals. In clinical settings and physiological conditions proven to be hemodynamically unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R-on-T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studies.
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PMID:Ventricular tachycardia and ventricular fibrillation in patients with short P-R intervals and narrow QRS complexes. 9 18

An attempt was made to derive a useful noninvasive index to evalute a change in myocardial contractile state using transcutaneous Doppler flow-velocity curve from the carotid artery. In 5 mongrel dogs and in 43 patients with various heart disease, Doppler flow velocity curves were obtained from the ascending aorta intravascularly using a Doppler catheter and/or from carotid artery transcutaneously using a Doppler probe. The first derivative of left ventricular pressure (dp/dt) and electrocardiogram (ECG) were recorded simultaneously. The following 3 indices were measured from the Doppler flow-velocity curves: (1) macimum acceleration of blood flow (dv/dt), (2) time from onset of ejection to peak flow (time-to-peak), (3) time interval between the beginning of Q wave of ECG to the peak of Doppler flow velocity curve (ECG Q-Doppler peak). Among these 3 indices, only ECG Q-Doppler peak demonstrated a significant correlation between the values measured intravascularly and transcutaneously. Also, only ECG Q-Doppler peak showed significant correlation with maximum of dp/dt (max dp/dt). Since ECG Q-Doppler peak showed correlation with heart rate, the difference between observed and predicted ECG Q-Doppler peak (delta ECG Q-Doppler peak) was calculated to exclude the effect of heart rate. Predicted value of ECG Q-Doppler peak was calculated from the regression equation between heart rate and ECG Q-Doppler peak in the separate experiments. There was significant correlation between delta ECG Q-Doppler peak and max dp/dt. In 15 patients with coronary artery disease and in 16 healthy subjects, delta ECG Q-Doppler peak and the other noninvasive method (systolic time intervals) were measured. Delta ECG Q-Doppler peak showed better result in the separation of 2 groups than by systolic timeintervals. It was concluded that delta ECG Q-Doppler peak is a useful index to evaluate the myocardial contractile state since this index is readily obtained noninvasively.
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PMID:Blood flow velocity in the carotid artery as a measure of myocardial contractility. 12 16

Eighty patients with various forms of heart disease were studied with the use of a newly developed ultrasonic system having 20 transducers arranged in a linear array. This system allows visualization of the heart in two dimensions in real time. All 15 patients with the mitral valve prolapse syndrome, 13 patients with mitral stenosis, five patients with pericardial effusion, four patients with atrial septal defect, and one patient with left ventricular dyssynergy were properly recognized with this system. One of five patients with hypertrophic myopathy and one of four patients with congestive myopathy were not recognized with this system. Criteria for the recognition of these system. Criteria for the recognition of these conditions are presented as well as the probable cause for false-positive and false-negative diagnoses in this series. Since only qualitative criteria were used, it was not possible to differentiate patients with coronary artery disease or patients with left ventricular volume overload from patients without cardiac pathology. The accuracy of this new system was judged against the clinical examination, conventional echocardiography, cardiac catheterization, and left ventricular angiography. It is assumed that the criteria for diagnosis developed during this study will be supplemented and the equipment improved in the future; however, the ease of operation of this system and the relative accuracy of diagnosis at this stage of its development are extremely interesting. It presents an excellent opportunity to obtain additional information about the cardiac patient without using invasive procedures and without risk.
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PMID:Diagnostic accuracy of an ultrasonic multiple transducer cardiac imaging system. 12 12

The ECG and Frank VCG were compared to the hemodynamic findings in 33 patients with idiopathic hypertrophic subaortic stenosis in whom cardiac catheterization had excluded concomitant valvular heart disease, congenital heart disease, or occlusive coronary artery disease. The patients were divided into two groups according to the absence (Group I) or presence (Group II) of left ventricular hypertrophy on the ECG and/or VCG. The 11 patients in Group I were found to have neither mitral insufficiency nor a resting left intraventricular gradient, and only six patients in whom mitral valve movement was visualized demonstrated systolic anterior movement of the anterior leaflet. The papillary muscles and left ventricular wall were either normal or only mildly hypertrophied in 10 of 11 Group I patients. Group II (22 patients) demonstrated either a resting left intraventricular gradient and/or mitral insufficiency in 18 patients. Twenty-one of the 22 patients showed systolic anterior movement of the anterior leaflet of the mitral valve on a cineangiogram and the papillary muscles and left ventricular wall were moderately to severely hypertrophied in 18 patients. These data suggest that specific hemodynamic and anatomic characteristics of hypertrophic subaortic stenosis may be predicted with reasonable accuracy from the ECG and VCG.
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PMID:Electrocardiographic and hemodynamic correlations in patients with idiopathic hypertrophic subaortic stenosis. 12 82

The mechanism of the electrocardiographic pattern termed left atrial enlargement was evaluated in 21 patients. Left atrial size and pressure as well as interatrial conduction were correlated with electrocardiographic left atrial enlargement using echocardiography, mean pulmonary capillary wedge pressure and activation time from the P wave to the coronary sinus. In the group as a whole only prolongation of interatrial conduction time was consistently related to the electrocardiographic pattern of left atrial enlargement; left atrial size or pressure was not predictably abnormal in patients with this pattern. Five patients had neither elevation of pulmonary capillary wedge pressure nor echocardiographic evidence of an enlarged left atrium. When the etiologic type of heart disease was analyzed, an enlarged left atrium correlated with electrocardiographic left atrial enlargement only in patients with rheumatic mitral valve disease (eight of nine patients). Elevated pulmonary capillary wedge pressure correlated with electrocardiographic left atrial enlargement in all four patients with cardiomyopathy. In patients with coronary artery disease the electrocardiographic pattern was unrelated to either left atrial pressure or volume overload. Thus, the electrocardiographic pattern termed left atrial enlargement appears to represent an interatrial conduction defect that can be produced by a variety of factors.
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PMID:Electrocardiographic left atrial enlargement. Electrophysiologic, echocardiographic and hemodynamic correlates. 14 Dec 2

Fifty patients with sustained ventricular tachycardia were studied by endocavitary recordings and programmed electrical stimulation. Of 29 patients in whom tachycardia could be initiated, 18 had chronic coronary artery disease and eight had no detectable heart disease. Of 35 patients in whom the tachycardia could be terminated by premature ventricular stimuli, 21 had chronic coronary artery disease and eight had no detectable heart disease. Initiation of tachycardia was facilitated in 18 of 21 patients by pacing the ventricle at the slowest possible pacing rate. An inverse relation was found between the prematurity of the tachycardia-initiating premature beat and the interval between the premature beat and the first beat of tachycardia, a finding suggestive of a re-entry mechanism. The role of the specific conduction system in initiation and during tachycardia remains unknown. Stimulation site was found to affect initiation and termination of tachycardia and width of tachycardia zone.
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PMID:Observations on mechanisms of ventricular tachycardia in man. 18 Nov 69

The effects of intravenously administered disopyramide phosphate were evaluated in seven patients with refractory ventricular tachycardia. All patients had organic heart disease, including acute infarction (three patients), chronic coronary artery disease (two patients) and cardiomyopathy (two patients). The severity of the heart disease was reflected in the advanced patient age (average 64 years) and the occurrence before disopyramide therapy of cardiac arrest in five patients and congestive heart failure in all seven patients. In five patients, disopyramide was given as a bolus injection, 2 mg/kg body weight, followed by an infusion of 20 to 40 mg/hour. The final two patients received 4 mg/kg divided as a bolus injection and an infusion over 1 hour followed by a 0.4 mg/kg infusion during the next hour. Intravenous administration of disopyramide resulted in more effective electrical stability in all patients and completely eliminated ventricular tachycardia in six. Recurrence of ventricular tachycardia was prevented in six patients with subsequent long-term oral administration of disopyramide. Possible dose-related cardiac pump depression occurred in two patients, but disopyramide was otherwise well tolerated. Therefore, these data document the therapeutic efficacy of disopyramide in the treatment of refractory life-threatening ventricular tachyarrhythmias.
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PMID:Efficacy of disopyramide phosphate in the treatment of refractory ventricular tachycardia. 32 16

Arteriosclerotic heart disease is a major cause of death in insulin-requiring juvenile diabetic patients treated for end-stage renal disease. Eleven consecutive diabetic patients without clinical evidence of coronary artery disease underwent complete cardiac evaluations, including coronary arteriography, as part of transplant recipient work-ups. Seven were women and four were men; their mean age was 32 (21 to 50 years). Angiographically, every patient had multifocal atherosclerotic coronary disease. Four of seven patients tested had positive-stress electrocardiograms. In this group of patients followed for a mean of 19.8 months, eight died. Of these deaths, six were due to coronary heart disease and another due to a stroke. In two patients who became clinically symptomatic, serial angiograms revealed progressive disease of the coronary circulation; in one case, despite normal renal allograft function and serum lipid levels. The mode of end-stage renal disease treatment, serum lipids or blood pressure control could not be linked to mortality. It is concluded that arteriosclerotic heart disease is common in diabetic patients with end-stage renal disease even when angina is absent. The natural history in this high risk population is an important consideration in the selection of patients for end-stage renal disease treatment.
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PMID:Natural history of asymptomatic coronary arteriographic lesions in diabetic patients with end-stage renal disease. 36 Aug 37

Heart disease continues to be a major cause of disablement and death in Canada. Elevated serum cholesterol concentrations, hypertension and cigarette smoking are among the standard risk factors associated with ischemic heart disease. Research attention has also been directed at the role of behavioural factors in the development of atherosclerosis and myocardial infarction. Experimental findings support a conceptual approach to the interplay of psychologic stress, the type A "coronary"-prone behaviour pattern and pathophysiologic mechanisms that have been implicated in the development of coronary artery disease. It is concluded that type A behaviour and stress contribute substantially to the pathogenesis of cardiovascular disease. However, assessment of the manner in which these two variables influence the pathophysiology of ischemic heart disease requires further research, with systematic examination of physiologic and biochemical processes. Potential strategies for modifying type A behaviour are reviewed. However, unequivocal support for the preventive efficacy of behavioural approaches must await future research.
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PMID:Behavioural prevention of ischemic heart disease. 36 Nov 91


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