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

Atrial fibrillation (AF) is a common arrhythmia, occurring in 0.4% of the general population. AF has been shown to be associated with left atrial enlargement, which is considered both a cause and a consequence of the arrhythmia. The aim of the study was to determine the influence of AF on changes in echocardiographically determined left atrial (LA) size, during 5 year follow-up period, in a population with well-controlled hypertension, free from structural heart disease, except mild left ventricle thickening, and with an absence of other potential causes of atrial enlargement. The study group, comprised of 81 patients with persistent AF, with underlying hypertensive heart disease, consecutively referred for elective direct current cardioversion. The mean age of the study population was 59.3+/-8.4 years (ranged from 43 to 80), a mean AF duration was 8.8+/-8.7 months (ranged from 1 to 30 months). The patients underwent two-dimensional echocardiography to determine left atrial size, before and 5 years after cardioversion. Twenty out of eighty-one cardioverted patients maintained sinus rhythm 5 years after cardioversion (25%). In this group anteroposterior LA dimension and LA volume decreased from a mean (+/-S.D.) 49.7+/-4.5 to 46.8+/-4.8 mm (-6%, p < 0.05) and from 103.6+/-28.8 to 91.1+/-18.3 cm2 (-9.2%, p < 0.05), respectively. Left ventricle ejection fraction increased from 52.8+/-6.3% to 60.0+/-4.0% (p < 0.05) and clinical stage improved in patients who maintained sinus rhythm through 5 years. In contrast, in the AF group, anteroposterior LA dimension and LA volume increased from 46.6+/-4.3 to 48.1+/-5.6 mm, and from 91.3+/-20 to 103+/-34 cm2 (by an average 3.3% and 14.3%, respectively), at the end of study. When divided into two groups: Imid R:II and III NYHA class, in AF patients LA volume increased by an 21.4% in the III NYHA class and 7.3% in the Imid R:II NYHA class. Left ventricular ejection fraction did not change between the two echocardiographic studies in the AF group (44.9+/-14.3% vs. 44.6+/-12.9%, Ns). In conclusion, it has been proved that AF occurring in patients with hypertensive heart disease causes a slow and progressive increase in LA size especially in patients in functional III NYHA class, and that the maintenance of sinus rhythm partially reverts the process of LA enlargement in patients with well-controlled hypertension, a history of AF and successfully treated for AF.
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PMID:Changes in left atrial size in patients with persistent atrial fibrillation: a prospective echocardiographic study with a 5-year follow-up period. 1586 Mar 82

Plasma B-type natriuretic peptide (BNP) levels have been reported to be elevated in various types of cardiac disorders and in precursors of CHF. To elucidate the potential ability of BNP testing to identify individuals with structural cardiac disease (ie, hypertensive heart disease, coronary heart disease, valvular heart disease) among community-dwelling elderly persons, cases which were positive on BNP testing were compared to those positive on ECG testing. In the initial phase, we performed plasma BNP measurements and ECG in 856 participants (age > or = 65 years) selected from a general population. From within this group, subjects with an abnormal ECG (n = 125) were selected according to the Minnesota code. Subjects with elevated BNP were selected independently on the basis of plasma levels (n = 112). In the next phase, subjects in both groups were invited to complete Rose's angina questionnaire and to undergo physical examination and transthoracic echocardiography. In this subject group (positive in ECG testing and/or BNP testing), the two tests had comparable sensitivity (65% versus 59%: NS) and specificity (40% versus 41%: NS) for identifying hypertensive heart disease (n = 17). For coronary heart disease (n = 12), the two tests had also comparable sensitivity (58% versus 42%: NS) and specificity (39% versus 41%: NS). However, for selection of valvular heart disease (n = 7), BNP testing had higher sensitivity than ECG testing (100% versus 14%; P < 0.01) with comparable specificity (43% versus 40%: NS). Several types of structural heart disease, in particular valvular heart disease, could be identified exclusively by BNP testing, suggesting that BNP measurement can make a significant contribution to screening for CHF precursors when used in combination with ECG in elderly populations.
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PMID:Comparison of positive cases for B-type natriuretic peptide and ECG testing for identification of precursor forms of heart failure in an elderly population. 1604 43

Diabetes mellitus is responsible for a spectrum of cardiovascular disease. The best known complications arise from endothelial dysfunction, oxidation, inflammation, and vascular remodelling and contribute to atherogenesis. However, the effects on the heart also relate to concurrent hypertensive heart disease, as well as direct effects of diabetes on the myocardium. Diabetic heart disease, defined as myocardial disease in patients with diabetes that cannot be ascribed to hypertension, coronary artery disease, or other known cardiac disease, is reviewed.
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PMID:Diabetic heart disease. 1615 78

Normal ejection fraction (EFs) is often equated with normal systolic function. However, midwall mechanics reveal systolic dysfunction in hypertensive heart disease accompanied by hypertrophic remodeling. Midwall mechanics are unstudied in patients with acute diastolic heart failure (HF). This study analyzed left ventricular (LV) midwall stress-shortening relations in 61 patients aged >60 years with hypertensive heart disease, HF, and normal EF. Sixty-one hypertensive patients (mean age 78 +/- 10 years) who presented with HF, each with an EF >50%, underwent echocardiography. Midwall mechanics were compared with those of 79 controls (mean age 75 +/- 8 years) without structural heart disease. Relative wall thickness (0.63 +/- 0.11 vs 0.46 +/- 0.10 mm) and LV mass (237 +/- 67 vs 177 +/- 57 g) were significantly greater in patients with HF compared with controls. Mean EFs were similar in patients with HF and controls (64 +/- 9% vs 67 +/- 9%). Although mean endocardial fractional shortening (35 +/- 7% vs 37 +/- 7%) was not significantly different, midwall shortening in patients with HF was significantly less compared with controls (16 +/- 2% vs 19 +/- 3%, p <0.05). Eighteen of the 61 patients with HF (30%) had midwall shortening that was <95% confidence intervals of the normal midwall stress-shortening relations. By this criterion, these patients had systolic dysfunction despite normal EF; they had smaller LV chambers (in dimension and volume), greater relative wall thickness, and smaller stroke volumes. In conclusion, almost 1/3 of patients hospitalized with diastolic HF had systolic dysfunction, characterized by abnormal midwall stress-shortening relations.
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PMID:Analysis of left ventricular systolic function using midwall mechanics in patients >60 years of age with hypertensive heart disease and heart failure. 1625 2

The problem of heart disease of unknown aetiology as it is found in the Nigerian environment is presented. The fact that it is nearly impossible on many occasions to make a conclusive diagnosis on clinical grounds alone of either endomyocardial fibrosis and heart muscle disease is discussed and the need for haemodynamic and angiographic studies to make the differentiation is stressed. The clinical, radiological, electrocardiographic, and haemodynamic features of each of the two varieties of "cardiomyopathy" is presented and the distinguishing features are emphasised. The occasional difficulty in differentiating heart muscle disease from hypertensive heart disease is discussed and the fact that the two differ distinctly on haemodynamic pressure studies is established. Previous published hypotheses regarding the aetiology of these cardiac conditions are discussed, and suggestions are made as to the lines of future research including virological studies and the possible myocardiopathic effect of some of the local traditional herbs.
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PMID:Myocardial disease in Nigerians. 1629 77

Experimental and population-based studies indicate that female gender and estrogens protect the cardiovascular system against aldosterone-induced injury. Understanding the function of estrogens in heart disease requires more precise information on the role of both estrogen receptor (ER) subtypes, ERalpha and ERbeta. Therefore, we determined whether selective activation of ERalpha or of ERbeta would confer redundant, specific, or opposing effects on cardiovascular remodeling in aldosterone salt-treated rats. The ERalpha agonist 16alpha-LE2, the ERbeta agonist 8beta-VE2, and the nonselective estrogen receptor agonist 17beta-estradiol lowered elevated blood pressure, cardiac mass, and cardiac myocyte cross-sectional areas, as well as increased perivascular collagen accumulation and vascular osteopontin expression in ovariectomized rats receiving chronic aldosterone infusion plus a high-salt diet for 8 weeks. Uterus atrophy was prevented by 16alpha-LE2 and 17beta-estradiol but not by 8beta-VE2. Cardiac proteome analyses by 2D gel electrophoresis, mass spectrometry, and peptide sequencing identified specific subsets of proteins involved in cardiac contractility, energy metabolism, cellular stress response and extracellular matrix formation that were regulated in opposite directions by aldosterone salt treatment and by different estrogen receptor agonists. We conclude that activation of either ERalpha or ERbeta protects the cardiovascular system against the detrimental effects of aldosterone salt treatment and confers redundant, as well as specific, effects on cardiac protein expression. Nonfeminizing ERbeta agonists such as 8beta-VE2 have a therapeutic potential in the treatment of hypertensive heart disease.
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PMID:Both estrogen receptor subtypes, alpha and beta, attenuate cardiovascular remodeling in aldosterone salt-treated rats. 1756 76

Gender differences in the development of cardiovascular disease suggested for a protective function of estrogens in heart disease. The negative or neutral outcome of clinical trials on hormone replacement therapy provides clear evidence that the role of female sex hormones in the cardiovascular system is more complex than previously thought. In particular, the function of estrogens can not be understood without detailed knowledge on the specific function of both estrogen receptor subtypes in the heart and in the vasculature. In here, we review recent studies on subtype selective ERalpha and ERbeta agonists in different animal models of hypertension, cardiac hypertrophy and vascular inflammation. The results indicate that the activation of specific ER subtypes confers specific as well as redundant protective effects in hypertensive heart disease that might ultimately translate into novel treatment options for hypertensive heart disease.
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PMID:Functional effects and molecular mechanisms of subtype-selective ERalpha and ERbeta agonists in the cardiovascular system. 1782 73

Hypertension is a major risk factor for developing cardiac hypertrophy and heart failure. Previous studies show that hypertrophied and failing hearts display alterations in excitation-contraction (E-C) coupling. However, it is unclear whether remodeling of the E-C coupling system occurs before or after heart disease development. We hypothesized that hypertension might cause changes in the E-C coupling system that, in turn, induce hypertrophy. Here we tested this hypothesis by utilizing the progressive development of hypertensive heart disease in the spontaneously hypertensive rat (SHR) to identify a window period when SHR had just developed hypertension but had not yet developed hypertrophy. We found the following major changes in cardiac E-C coupling during this window period. 1) Using echocardiography and hemodynamics measurements, we found a decrease of left ventricular ejection fraction and cardiac output after the onset of hypertension. 2) Studies in isolated ventricular myocytes showed that myocardial contraction was also enhanced at the same time. 3) The action potential became prolonged. 4) The E-C coupling gain was increased. 5) The systolic Ca(2+) transient was augmented. These data show that profound changes in E-C coupling already occur at the onset of hypertension and precede hypertrophy development. Prolonged action potential and increased E-C coupling gain synergistically increase the Ca(2+) transient. Functionally, augmented Ca(2+) transient causes enhancement of myocardial contraction that can partially compensate for the greater workload to maintain cardiac output. The increased Ca(2+) signaling cascade as a molecular mechanism linking hypertension to cardiac hypertrophy development is also discussed.
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PMID:Hypertension-induced remodeling of cardiac excitation-contraction coupling in ventricular myocytes occurs prior to hypertrophy development. 1787 27

Resting cardiac function is a poor indicator of functional cardiac reserve that is invoked during exercise. The objective of this study was to investigate the relationship between functional cardiac reserve and systemic vascular resistance (SVR) using an ambulatory radionuclide monitoring system (the Vest system) in patients with heart disease. The study population consisted of 29 patients (all male [mean +/- SD age, 63 +/- 10 years]), 23 with coronary artery disease, 3 with dilated cardiomyopathy, and 3 with hypertensive heart disease. All patients underwent cardiopulmonary stress testing using a ramped treadmill protocol and the Vest system. The anaerobic threshold (AT) was autodetermined using the V-slope method. Systemic vascular resistance was calculated using the mean blood pressure and cardiac output as determined using the Vest system parameters. All patients exercised beyond the AT until exhaustion. Resting left ventricular ejection fraction, peak ejection ratio, and peak filling ratio increased with the AT (P < .01 for all). Resting SVR decreased with the AT (P < .01). The percentage changes from rest to the AT in SVR correlated with those from rest to the AT in ejection fraction, peak ejection ratio, and peak filling ratio (r = -0.735, r = -0.510, and r = -0.697, respectively; P < .01). These findings indicate that SVR as recorded using the Vest system is a good determinant of functional cardiac reserve in patients with heart disease. Therefore, cardiopulmonary function testing combined with the Vest system is a good modality for the evaluation of functional cardiac reserve.
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PMID:Systemic peripheral vascular resistance as a determinant of functional cardiac reserve in response to exercise in patients with heart disease. 1787 59

Coronary heart disease and chronic heart failure are common and have an increasing frequency. Although interventional and conventional drug therapy may delay ventricular remodelling, there is no basic therapeutic regime available for preventing or even reversing this process. Chronic coronary artery disease and heart failure impairs quality of life and are associated with subsequent worsening of the cardiac pump function. Numerous studies within the past few years have been demonstrated, that the intracoronary stem cell therapy has to be considered as a safe therapeutic procedure in heart disease, when destroyed and/or compromised heart muscle must be regenerated. This kind of cell therapy with autologous bone marrow cells is completely justified ethically, except for the small numbers of patients with direct or indirect bone marrow disease (e.g. myeloma, leukaemic infiltration) in whom there would be lesions of mononuclear cells. Several preclinical as well as clinical trials have shown that transplantation of autologous bone marrow cells or precursor cells improved cardiac function after myocardial infarction and in chronic coronary heart disease. The age of infarction seems to be irrelevant to regenerative potency of stem cells, since stem cells therapy in old infarctions (many years old) is almost equally effective in comparison to previous infarcts. Further indications are non-ischemic cardiomyopathy (dilative cardiomyopathy) and heart failure due to hypertensive heart disease.
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PMID:The therapeutic potential of stem cells in heart disease. 1818 53


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