Bibliography. Current world literature. Valvular heart disease.
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To evaluate the importance of oral maintenance digoxin therapy in chronic congestive heart failure (CHF), 24 patients in sinus rhythm on maintenance digoxin for documented CHF were studied prospectively on and off the drug. The average duration of therapy was 39 months (range 2 to 180). All 24 patients had documented coronary artery disease (CAD): 22 were in New York Heart Association functional class III and 2 in class II. Twenty-one patients (88%) were receiving diuretic or vasodilator therapy, or both, before digoxin discontinuance. At 1 month off digoxin and with no increase in doses of other medications excepting minor increases in antianginal therapy in 2 patients, no difference was observed in the group as a whole in symptoms, resting heart rate, arterial blood pressure, physical findings, weight, cardiothoracic ratio, radiographic signs of pulmonary congestion, radionuclide left ventricular ejection fraction (LVEF), duration of symptom-limited treadmill exercise (14 patients), or CHF score, compared with evaluation during maintenance digoxin therapy. Similar results were obtained in a subgroup of 9 patients with a resting LVEF less than 0.35 (0.27 +/- 0.02; mean +/- standard error of the mean). Six patients had a decrease and 5 patients an increase in LVEF of greater than or equal to 0.05 units after cessation of digoxin. Off digoxin, the CHF score increased by only 1 point in 2 patients, but also decreased in 2 patients. Thus, in this study population comprised of patients with CAD with documented CHF, most of whom were receiving diuretics or vasodilators, or both, digoxin withdrawal had no adverse clinical or hemodynamic effects.
In 24 patients (pts) with proven coronary artery disease, stable angina pectoris (AP) and elevated pulmonary artery pressure (PAP) during bicycle exercise, the acute and chronic (4 and 8 months) effects of several long-acting nitrates in different dosages: 50-300 mg pentaerythrityltetranitrate (PETN) or 40-120 mg isosorbide dinitrate (ISDN) were evaluated in comparison to sublingual nitroglycerin. Nitroglycerin was about 30%-40% more effective than PETN and ISDN with regard to pulmonary artery pressure at exercise. Beneficial effects of both long-acting nitrates were shown with regard to the number of anginal attacks, nitroglycerin consumption, and ST-segment depression both during short- and long-term treatment. Both nitrates decreased exercise pulmonary artery pressure by 15%-20%, at acute testing and during chronic therapy. There was no difference with respect to the long-term effects of both long-acting nitrates. However, more side-effects were observed during ISDN treatment. There were no signs of nitrate tolerance development with the therapy schedules under investigation.
Mortality and morbidity from ischaemic heart disease (IHD) was studied in 5404 Finnish males aged 35-64 years who had been hospitalised for alcohol-related disease in 1972 without any admissions for IHD during that same period. By record-linkage, morbidity and mortality were followed up to the end of 1975. The mortality of patients with alcohol-related diseases was compared to 1120 patients with acute appendicitis by calculating indirectly age-standardised mortality ratios (SMR). The mortality and morbidity of 5963 patients with acute myocardial infarction or angina pectoris was also studied. The following SMRs for IHD mortality, non-fatal-IHD-hospitalisation and for mortality from all causes respectively, were found: acute myocardial infarction 11.6, 7.2 and 7.2; alcohol intoxication 6.0, 4.5 and 4.5; angina pectoris 5.2, 10.5 and 3.4; liver cirrhosis 2.2, 2.5 and 11.8; alcoholism 1.9, 1.9 and 3.6; pancreatitis 1.8, 1.2 and 4.4; alcohol psychosis 1.7, 2.5 and 4.2. IHD mortality and morbidity appeared to be more prevalent in patients hospitalised with alcohol intoxication than in patients with other alcohol-related diseases. This suggests that rapid drinking predisposes both to serious intoxication and to fatal disturbances of cardiac rhythm.
Forty-seven consecutive patients (mean age 61 +/- 8 years) referred for cardiac catheterization due to moderate to severe aortic (n = 30) or mitral (n = 17) valvular heart disease were examined by technetium-99m isonitrile tomography together with a high-dose dipyridamole infusion (0.7 mg/kg) and handgrip stress. Tomography did not identify coronary artery disease (CAD) in 3 of the 21 patients with angiographically proven disease (sensitivity 86%) and suggested false positive results in 5 of the 26 without the disease (specificity 81% and negative predictive accuracy 88%). No patient without angina pectoris and with negative scintigraphy (n = 14) had angiographically significant (greater than or equal to 50% diameter stenosis) CAD. Overall vessel sensitivity was 63%, and specificity was 92%. The frequency of side effects during the dipyridamole-handgrip test was only 7%. No serious complications occurred during stress tests. Thus, technetium-99m isonitrile tomographic imaging, together with high-dose dipyridamole and handgrip exercise, is a useful noninvasive method in excluding significant CAD in patients with valvular heart disease.
Adults with congenital heart disease represent a new and growing population of patients who pose a challenge to both medicine and nursing. The purpose of this study was to identify the educational needs of adults with congenital heart disease. The study used a prospective, cross-sectional, case-control study design and enrolled 124 adults with congenital heart disease and 124 matched healthy controls. Adults with congenital heart disease were more likely to report living at home with parents and less likely to be employed compared with healthy controls. When those adults with acyanotic and cyanotic congenital heart disease were compared, acyanotic adults were twice as likely to be employed. Additionally, several areas of educational needs were identified in this study for adults with congenital heart disease.
The Northwick Park Heart Study found that elevation of factor VII in middle-aged subjects was an independent risk factor for subsequent ischemic heart disease. The present study was designed to determine whether factor VII elevation is present at a younger age and whether zymogen or activated factor VII is responsible for this elevation. A group of 20 asymptomatic first degree relatives (mean age 34.9 years) of patients with premature ischemic heart disease were compared with 15 age-matched normal subjects at low risk of ischemic heart disease and 15 older subjects with established ischemic heart disease (mean age 49.7 years). Factor VII procoagulant, coupled amidolytic and antigenic assays, as well as fasting serum triglyceride and cholesterol assays, were performed on all three groups. Factor VII antigen and coagulant activity was significantly elevated in first degree relatives, as was factor VII antigen in the patients with ischemic heart disease. The increased factor VII level in these subjects was caused by elevated factor VII zymogen, not activated factor VII. The results of this study, combined with those of previous studies, suggest that factor VII may be a useful additional marker of the risk for ischemic heart disease and merits further investigation.
BACKGROUND: It has been suggested that cytomegalovirus infection increases the risk of ischemic heart disease. Both cytomegalovirus and ischemic heart disease are common after renal transplantation, suggesting a possible causal association in this population. METHODS AND PATIENTS: We studied 1004 consecutive renal transplants with no prior history of ischemic heart disease and grafts that functioned at least 12 months. We performed univariate and multivariate analyses to examine the effect of cytomegalovirus disease and other risk factors (measured during the first posttransplant year) on the development of primary ischemic heart disease events after the first posttransplant year. RESULTS: More than 1 year after transplantation, 116 patients (11.6%) experienced their first ischemic event (75 myocardial infarction, 12 percutaneous angioplasty, 18 bypass grafting, and 11 deaths). Patients with ischemic heart disease were more likely to have known risk factors (age, diabetes, smoking, hypercholesterolemia, systolic blood pressure, low serum albumin, and acute rejections). However, the incidence of cytomegalovirus disease was not different for those with or without ischemic heart disease (36.2% vs. 31.1%). Moreover, a similar proportion of those with and without ischemic heart disease (19.8% vs. 15.5%) had a rise in cytomegalovirus antibodies during follow-up. By multivariate analysis, risk factors for ischemic heart disease (P<0.05) were age, diabetes, smoking, low serum albumin, and two or more acute rejections during the first year. Cytomegalovirus disease was not associated with ischemic heart disease events: unadjusted relative risk=1.14 (95% confidence interval 0.78-1.67, P=0.485). After adjusting for multiple risk factors, the relative risk was 0.91 (0.60-1.37, P=0.657). CONCLUSION: These data suggest that cytomegalovirus disease is not a significant risk factor for the development of primary ischemic heart disease after renal transplantation.
The predictive value of electrocardiographic (ECG) abnormalities at baseline for subsequent risk of fatal and total coronary heart disease (CHD) was analyzed in a 12-year follow-up of 7682 men in the Honolulu Heart Program aged 45-68 who were free of CHD at baseline. Univariate analysis showed that men with major or minor ECG abnormalities, ST depression, high R wave, T-wave inversion, left ventricular hypertrophy or strain and premature ventricular contractions had considerably higher (2-10 fold) CHD incidence rates than those with normal ECG. When blood pressure, cigarette smoking, body mass index, alcohol use, physical activity, serum glucose, serum cholesterol, serum uric acid, age and years lived in Japan were taken into consideration through multivariate analysis, the ECG abnormalities retained significant associations with fatal and total CHD. This study demonstrated that resting ECG abnormalities were independent predictors of both total and fatal CHD.
In valvular heart disease, there is a different radionuclide angiographic pattern in each of three left-sided valve abnormalities: pressure overload (aortic stenosis), volume overload (aortic or mitral regurgitation) and inflow obstruction (mitral stenosis). In pressure overload, the left ventricle is usually normal in size or minimally dilated. The ejection fraction may be normal, increased or decreased. In volume overload, there is left ventricular dilatation with a normal or reduced ejection fraction at rest. Scans may be performed during exercise to unmask abnormalities of ventricular function not evident at rest. In inflow obstruction, left ventricular function is usually normal but may be depressed. Right ventricular function may be abnormal secondary to pulmonary hypertension. Radionuclide angiography in valvular heart disease evaluates the impact of the valve abnormality on cardiac chamber size and function, which is useful in managing the patient, in determining the prognosis and in evaluating the success of valve surgery. Thallium-2-1 imaging evaluates regional myocardial blood flow and cell integrity and can be used to assess associated coronary artery disease.
The presence of calcified coronary artery plaque has shown variable association with clinical coronary heart disease (CHD), particularly after adjustment for other risk factors. From 2002 to 2004, as part of the National Heart, Lung, and Blood Institute's Family Heart Study, coronary artery calcium (CAC) scans by 4-slice multidetector computed tomography were performed in 3,359 subjects, including 389 with clinically diagnosed CHD. Among these was a cohort of 2,254 patients who had been asymptomatic at an initial examination 7 to 9 years previously (1994 to 1996), with 111 who had developed newly diagnosed, nonfatal CHD since the initial examination. In cross-sectional analyses, we examined associations between CAC and CHD in the entire group and in the subgroup seen at the initial examination. In the 2 sets of analyses, odds ratios for CHD ranged from approximately 4 in those with CAC scores of 100 to 199 (p <0.01) to >20 in those with CAC scores >/=1,000 (p <0.0001) compared with those with no measurable CAC. This steep gradient of risk persisted after adjustment for risk factors. A quantitative CHD family history score was significantly associated with CHD even after adjusting for all standard risk factors and including CAC in the model. In conclusion, CAC was strongly associated with CHD even after adjustment for standard risk factors and family history contributed independently to CHD risk.
The heart has a limited potential to synthesize fatty acid (FA), and, therefore, FA is supplied from several sources: lipolysis of endogenous cardiac triglyceride (TG) stores or from exogenous sources in the blood. Lipoprotein lipase (LPL), synthesized in cardiomyocytes, catalyzes the breakdown of the TG component of lipoproteins to provide FA to the heart. It is the vascular endothelial-bound LPL that determines the rate of plasma TG clearance, and, hence, it is also called heparin-releasable (HR) "functional" LPL. Functional LPL is regulated by numerous dietary and hormonal factors and is sensitive to pathophysiological alterations like those observed during diabetes. In this condition, absolute or relative lack of insulin impairs cardiac glucose transport and oxidation, resulting in FA becoming the preferred means of energy supply. To make available this increased requirement of the heart for FA, the diabetic heart upregulates its luminal LPL activity by posttranslational mechanisms. Chronically elevated cardiac LPL can result in abnormal FA supply and utilization by the heart tissue that could potentially initiate and sustain cardiac dysfunction during diabetes. As effective blood glucose control is difficult during diabetes, it is conceivable that a parallel increase in functional cardiac LPL activity may predispose people with diabetes to premature death from cardiac disease. By gaining more insight into the initial metabolic processes in the diabetic heart, we can attempt to piece together a part of the cascade of events leading to diabetic heart disease.
The relationships of three measurements of the factor VIII/von Willebrand factor (VWF) complex (factor VIII activity, FVIIIc (one-stage assay); VWF antigen, VWF Ag (ELISA); and VWF activity, VWF act, measured by a recently-developed ELISA) to major ischaemic heart disease (IHD) events were studied in 1997 men aged 49-65 years, in the second phase of the Caerphilly Heart Study. These variables were related using logistic regression analysis to myocardial infarction or IHD death, which occurred in 129 men during an average follow-up period of 61 months. All three measurements were highly correlated (r = 0.63-0.77), and each was significantly associated with incident major IHD on univariate analyses (relative odds in highest fifth compared to lowest fifth, 1.68-1.90; P = 0.028-0.006) and on multivariate analyses adjusting for major IHD risk factors and for baseline IHD. Neither FVIIIc nor VWF act was significantly related to incident IHD following adjustment for VWF Ag. We therefore suggest that the associations between these three measurements of the factor VIII/VWF complex and incident IHD might have at least three explanations: VWF Ag is a marker of arterial endothelial disturbance; VWF act promotes platelet adhesion/aggregation and hence the platelet component of arterial thrombosis; and FVIIIc promotes fibrin formation and hence the fibrin component of arterial thrombosis.