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

Sudden cardiac death is defined as death due to a primary cardiac cause or mechanism, occurring within one hour of the onset of acute illness in a person thought to be free of, or with symptomatically mild, heart disease, or simply prehospital death. Of persons dying suddenly, 90% have coronary artery disease, less commonly, dilated cardiomyopathy or hypertrophic cardiomyopathy, preexcitation syndrome, long QT-syndrome, conduction disturbances, congenital or valvular heart disease as well as cardiac tamponade are responsible. In the USA, the incidence of sudden cardiac death is approximately 450,000 per year, in the Federal Republic of Germany the number lies at about 70,000 to 80,000. The most important risk factors for sudden cardiac death are impaired left ventricular ejection fraction, myocardial ischemia and arrhythmias. In general, sudden cardiac death is caused by ventricular fibrillation which arises mainly by degeneration of ventricular tachycardia (VT). The terminal arrhythmia, it is assumed, is precipitated by premature ventricular beats originating in an arrhythmogenic substrate. MEDICAL ANTIARRHYTHMIC TREATMENT IN PATIENTS WITH CORONARY ARTERY DISEASE AFTER MYOCARDIAL INFARCTION: STUDIES WITH CLASS I DRUGS: The results of nine large, randomized , controlled studies are available in which the mortality of patients on antiarrhythmic treatment has been studied (Table 1). Two studies each were carried out with aprindine, phenytoin, mexiletine and tocainide as well as one study with endainide, flecainide or morizicine. With the exception of the CAST study, no study showed a significant difference between treated patients and the control group with respect to mortality or incidence of sudden cardiac death. The CAST study was terminated after ten months because the administration of flecainide and encainide led to overall mortality of 7.7% vs. 3.0% in the control group and the rate of sudden cardiac death at 4.5% was significantly higher in the treatment group than the 1.2% incidence found in controls (Table 2). For nearly all of the studies described, the patient groups were not sufficiently large and subgrouping according to patient characteristics was not carried out such that possibly, inhomogeneity of the entire collective may not have been recognized precluding identification of some individuals who may have shown benefit from antiarrhythmic treatment. The necessity for treatment in many of those receiving drugs is questionable since generally the rhythm profile of the patients was not taken into consideration for the decision to treat. Proarrhythmic effects, accordingly, were also not assessed. Individual treatment and dosage adjustment by monitoring with effectiveness criteria was carried out in one study only in which, even here, criteria for effectiveness were arbitrarily capable of eliciting antiarrhythmic actions. Calculation of mortality rates was carried out on the basis of the total number of deaths in the respective groups without taking into consideration that by the end of the study, in the treatment group the medication had been discontinued in up to 40% of the patients. STUDIES WITH CLASS II DRUGS: For treatment with beta-receptor blockers there are 15 large, controlled, randomized, long-term studies available in which total mortality and the incidence of sudden cardiac death were studied.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Can sudden cardiac death be prevented by treatment with anti-arrhythmia drugs?]. 218 95

These findings permit the following conclusions on cardiac changes induced by high-performance sports and high levels of training. Sinus bradycardia and AV block can frequently be observed in athletes, but they do not require attention as long as they are asymptomatic or do not produce pauses exceeding 4 seconds. Persistent rather than transient second-degree AV block or Mobitz second- or third-degree AV block is an extremely unusual finding even in athletes and should be considered a sign of organic lesions until proved otherwise. Supraventricular and AV node ectopic beats are not more frequent in athletes than in the general population except for atrial fibrillation. WPW syndrome is of particular importance, since rapid conduction to the ventricle via the accessory AV pathway is possible, especially if there is a tendency toward atrial fibrillation. Likewise caution is required in athletes with hypertrophic cardiomyopathy. Here hemodynamic deterioration must be anticipated with the occurrence of supraventricular tachycardia. Simple ventricular arrhythmias occur among athletes with the same frequency as in the general population, but they usually disappear with exercise. The occurrence of complex ventricular forms of arrhythmia should always prompt cardiologic examination in search of underlying cardiac disease, particularly hypertrophic or dilated cardiomyopathy. The presence of ventricular arrhythmias without evidence of underlying heart disease does not indicate a special or increased risk of sudden cardiac death. A higher incidence of right and/or left ventricular hypertrophy, exercise-reversible ST elevation, and exercise-reversible changes in T waves (T negativity, sharp and/or excessive T waves) can be considered physiologic changes in the ECGs of athletes. These changes correlate closely with the type of sports activity and degree of training and are reversible when the activity is stopped. Horizontal ST segment depression are by contrast very rare in athletes and should always be clarified by cardiologic examination. Exercise-induced sudden cardiac death in athletes is unusual without preexisting heart disease. The cause of sudden cardiac death among athletes less than 40 years of age can be predominantely ascribed to congenital heart diseases (such as hypertrophic cardiomyopathy or coronary anomalies). In athletes more than 40 years of age and with increasing age, coronary heart disease is the most frequent autopsy finding. A corresponding risk stratification should take these partial dangers into account.
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PMID:ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance. 219 78

A young woman with humeroperoneal muscular dystrophy and contractures received a heart transplant for a severe dilated cardiomyopathy. Cardiac histopathology consisted of myocyte hypertrophy, interstitial fibrosis, and nuclear hyperchromaticity without mitochondrial abnormalities. Myopathy and heart disease were not clinically evident in her family, although three relatives had unexplained shortened Achilles tendons without weakness. Tendon contractures may be a partial expression of this myopathic disorder, suggesting an autosomal dominant inheritance with variable penetrance. A muscular dystrophy clinically similar to that of the Emery-Dreifuss (EDMD) type can thus occur in women. Rather than the cardiac arrhythmias typical of EDMD, a dilated cardiomyopathy may occur and present with severe congestive heart failure. This is the first report of cardiac transplantation in such a case.
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PMID:Cardiac transplantation in female Emery-Dreifuss muscular dystrophy. 223 Aug 49

There are obviously several causes of myocardial dysfunction but energy deficiency of the myocytes may play a significant role and probably is a common mechanism during the progression of myocardial failure. Theoretically, a poor utilization efficiency of oxygen may be due to exhaustion of the myocardial stores of bioenergetics. In this report the authors review their biochemical results from measurements of coenzyme Q10 (CoQ10) levels in blood and human endomyocardial biopsies using an HPLC method from patients with suspected myocardial disease (n = 45). The levels of CoQ10, which has a key role in the respiratory chain and the synthesis of ATP, was found to be significantly decreased in various groups of patients with myocardial failure (dilated and restrictive cardiomyopathy and alcoholic heart disease) as compared to "normal" myocardium (0.42 +/- 0.04 micrograms/mg dry weight). The deficiency of CoQ10 was more pronounced with increasing symptoms; e.g. patients with dilated cardiomyopathy in NYHA Classes III and IV had lower tissue CoQ10 content than those of Classes I and II (0.28 +/- 0.04 vs. 0.37 +/- 0.06 micrograms/mg, p less than 0.001). Nearly two thirds of a series of 40 patients in severe heart failure (Classes III and IV) treated with CoQ10, 100 mg daily, in an open, controlled design showed subjective and objective improvement. Clinical responders were 69% and 43% of patients with cardiomyopathy and ischaemic heart disease, respectively. The results suggest that CoQ10 is a novel and effective breakthrough in heart-failure therapy and it appears safe, as no adverse reactions were registered. The through in heart-failure therapy and it appears safe, as no adverse reactions were registered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coenzyme Q10: clinical benefits with biochemical correlates suggesting a scientific breakthrough in the management of chronic heart failure. 227 93

The proliferation of transplant programs has not been paralleled by a similar increase in the availability of organ donors. This has significantly prolonged the waiting period and consequently has resulted in increased mortality of the patients with end-stage heart disease who are awaiting transplantation. Between 1984 and 1987, 104 orthotopic heart transplants were performed at Loyola University Medical Center. During the same period, 25 patients died while waiting for a suitable donor. To reduce the mortality of our patients waiting for transplantation, we began using the total artificial heart and a ventricular assist device as a bridge to transplantation in 1988. Of 29 patients who underwent transplant procedures in 1988, 18 required either a total artificial heart (15) or a ventricular assist device (3) as a bridge to transplantation. The underlying heart conditions were ischemic cardiomyopathy (11), dilated cardiomyopathy (5), giant cell myocarditis (1), and allograft failure (1). The average duration of mechanical support was 10 days (range, 1 to 35 days). Seventeen of the supported patients had successful transplants. One patient had brain death and did not receive a heart transplant. Of the 17 patients who survived surgery, two died within 30 days: one at 17 days because of acute rejection, the other at 14 days because of a cerebral vascular event. Fifteen patients (83%) were long-term survivors. Nine of the supported patients required reoperation because of bleeding after device implantation. There was no mediastinal or incisional infection. While the mechanical device was in place, the activated clotting time was maintained between 170 and 200 seconds with the administration of heparin (400 to 1000 units per hour).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of the total artificial heart and ventricular assist device as a bridge to transplantation. 227 1

To evaluate the role of orthotopic cardiac transplantation for infants with lethal cardiac disease, we reviewed the results from our first 25 patients. Data on the donors were also reviewed to define the characteristics of a successful cardiac donor. Patients had transplants between November 1985 and November 1988. Several primary cardiac diagnoses were indications for transplantation, including congestive cardiomyopathy, hypoplastic left-heart syndrome, and other types of native and postoperative complex congenital heart diseases. The ages ranged from birth to 7 months. Of 25 patients, 21 are still alive (84% survival rate) with follow-up from 4 to 40 months. No late deaths have occurred. Long-term immunosuppression was accomplished with cyclosporine and azathioprine. Rejection surveillance was performed noninvasively; only one child required an endomyocardial biopsy. Donors died from a variety of traumatic and metabolic causes, including sudden infant death syndrome. The majority (72%) of donors had a history of cardiac arrest requiring cardiopulmonary resuscitation. One third were receiving inotropic support at the time of cardiac evaluation. We conclude that orthotopic cardiac transplantation is an effective therapy for infants with lethal heart disease. A larger donor pool is required, and many dying infants, despite cardiac arrest and resuscitation, would be suitable donors.
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PMID:Cardiac transplantation in infancy: donors and recipients. Loma Linda University Pediatric Heart Transplant Group. 229 99

We report our experience of myocardial scintigraphy with 201thallium (201Tl) in 52 children, aged 4 days to 18 years, in which 80 studies were made primarily to demonstrate or exclude impaired myocardial perfusion. For analysis, the patients were divided into the following eight groups: group I, coronary artery malformations (five patients); group II, Kawasaki's syndrome (six patients); group III, arterial switch operation (seven patients); group IV, dilated cardiomyopathy (18 patients); group V, hypertrophic cardiomyopathy (four patients); group VI, myocardial dysfunction after surgery for congenital heart disease (five patients); group VII, pulmonary atresia (three patients); and group VIII, miscellaneous (four patients). Myocardial scintigraphy was performed with a planar or tomographic technique at rest or after exercise (four patients). Isotope-uptake defects, indicating impaired myocardial perfusion, were present in 14 patients, including small infants. Defects were seen in all groups except those with hypertrophic cardiomyopathy and pulmonary atresia. The absence of such defects in several of the patients with Kawasaki's syndrome was particularly valuable as it made coronary angiography unnecessary. In the other groups of patients myocardial scintigraphy was a valuable adjunct to other investigations.
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PMID:Myocardial scintigraphy with 201thallium in pediatric cardiology: a review of 52 cases. 230 77

Abnormalities of left ventricular (LV) filling may occur prior to systolic dysfunction in patients with both coronary and noncoronary heart disease. To determine the incidence of diastolic dysfunction and to assess the relationship of such dysfunction to systolic performance, we measured systolic and diastolic function at rest in a series of healthy volunteers (n = 10) and in patients with cardiovascular disease (n = 42). Twenty patients had coronary artery disease (CAD) with prior myocardial infarction, six patients had CAD without myocardial infarction, and the remaining 16 patients had a variety of noncoronary heart diseases, including valvular heart disease, dilated cardiomyopathy, and hypertensive disease. The 42 patients manifested a wide variation in LV systolic function (ejection fractions ranged from 6% to 65%). Patients with reduced LV ejection fraction (EF) manifested a reduction in cardiac output and peak ejection rate proportionate to the reduction in EF. Diastolic function showed a fall in LV peak (PFR) and average (AFR) filling rates; these were reduced in proportion to the fall in EF. Heart rate was an insensitive index of the magnitude of impairment of LV systolic function. These data suggest that measurements of diastolic function do not provide additional information in patients with impaired systolic function.
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PMID:Evaluation of left ventricular diastolic function using an ambulatory radionuclide monitor: relationship to left ventricular systolic performance. 236 May 21

Left ventricular luminal changes were examined by percutaneous fiberoptic angioscopy in 13 patients with dilated cardiomyopathy and in four patients with acute myocarditis. Angioscope-guided endomyocardial biopsy was also performed in six patients with dilated cardiomyopathy and in two with acute myocarditis. A balloon-tipped guiding catheter (9F) was introduced through the right femoral artery into the left ventricle, the balloon was inflated, and a 1.6 or 4.3F fiberscope was introduced through the catheter into the ventricle so as to locate the fiberscope tip at the tip of the catheter shaft. The balloon was then pushed against the desired portion of the ventricle and warmed saline was infused to observe the luminal changes. In contrast to the patients without organic heart disease whose left ventricular luminal surface was brown in color, the luminal surface was white or light yellow in four, light brown in one, bluish-white in one, with white and brown portions distributed in a mosaic pattern in four, and it was reddish brown in the remaining one patient with dilated cardiomyopathy. Mural thrombi were observed in two of the patients. The luminal surface was light brown in one, reddish brown in one, rose in one, and red in one patient with acute myocarditis. Thrombi and scattered bleeding were observed in two and one of these patients, respectively. The changes in luminal coloration in patients with dilated cardiomyopathy and acute myocarditis had no obvious relation to left ventricular volume and ejection fraction. Angioscope-guided biopsy revealed that the white and light yellow portions were due to endocardial fibrosis, that the endocardia of brown portions were not fibrotic, and that the myocardium in the red portions contained mononuclear cells, indicating inflammation. The results indicate that the angioscopic features of the left ventricular luminal surface were not uniform in patients with dilated cardiomyopathy or in those with acute myocarditis, and that angioscopy can be used as a guiding tool for endomyocardial biopsy.
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PMID:Percutaneous fiberoptic angioscopy of the left ventricle in patients with dilated cardiomyopathy and acute myocarditis. 238 3

Prognostic significance of repetitive ventricular premature contractions (RVPC) were evaluated retrospectively in 452 patients studied with a 24 hours continuous electrocardiographic monitoring (Holter System). The patients were analysed in two groups: Group 1.- 199 patients; with primary heart disease: previous myocardial infarction (MI) in 114 patients, angina pectoris (AP) in 29 cases, congestive cardiomyopathy in 19 cases (COCM); hypertensive heart disease (AHCD) in 14 cases, Atherosclerotic heart disease (AEC) with conduction disturbance and without angina pectoris 23 cases. Group 2.- 253 patients without heart disease. Two different types of RVPCs were defined: Type A: as the occurrence of self-terminating two (coupled) or multifocal. RVACs Type B: Self limited ventricular tachycardias or "R on T phenomena". Forty patients of group 1 had RVPCs (23 type A and 17 type B) and 22% of them had sudden death (SD). Among 199 patients with structural heart disease, 74 had congestive heart failure (CHF) and 12 of these had RVPCs. 83% of patients with RVPCs died suddenly. No patients with CHF and without RVPCs had SD. In group 2 (without heart disease no patients died on the follow up, and 6% of them had RVPCs (68% type A and 32% type B). Coronary arteriographic and ventriculographic findings were reviewed in 92 patients with previous MI. In the patients followed 40 has RVPCs, and 9 of them had SD. Those 4 cases were cases of MI (25% of the patients with MI having RVPCs), 4 (25%) with COCM, and 1 (2.5%) with hypertensive cardiac disease. Thus, patients with MI or COCM had higher incidence of RVPCs, so they are at a high risk for sudden cardiac death.
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PMID:[Predictive value of sudden death in repetitive ventricular extrasystole]. 242 18


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