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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Data on the prognostic implications of left ventricular hypertrophy (LVH) in the Framingham Study based on routine ECG, echocardiogram (ECHO) and X-ray determination with 36 years of follow-up indicate that LVH has emerged as a powerful indicator of rapidly evolving lethal atherosclerotic disease, whether determined by ECG, ECHO or X-ray. Cardiovascular morbidity and mortality increase progressively with left ventricular muscle mass from lowest to highest values. The ECG and X-ray versions of LVH each independently contribute to the risk of cardiovascular events; each adds to the risk associated with the other, and those with both are at greater risk than those with either alone. Risk ratios associated with ECG-LVH are substantial and are greatest for cardiac failure and stroke, but coronary disease is the commonest and most lethal sequela. LVH is reversible, the anatomical variety more so than ECG-LVH, and reversal of this toward normal appears to confer greater benefit for the anatomical rather than the ECG manifestation of LVH. The risk of cardiovascular disease associated with LVH is not uniform, varying widely depending not only on whether there is concomitant ECG and anatomical evidence of hypertrophy but also on the associated hypertension, glucose intolerance, lipid profile and cigarette smoking habit. This suggests that there is much to be gained in correcting those associated risk factors which also promote the development of LVH.
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PMID:Left ventricular hypertrophy and mortality--results from the Framingham Study. 130 Dec 57

Effects of chronic heart failure upon receptor binding and cardiac function were studied in mongrel dogs. Heart failure was induced by three to seven, graded, sequential, intracoronary microembolizations performed 1 to 3 weeks apart. Depressed systolic and diastolic left ventricular function, reduced cardiac output, increased systemic vascular resistance, increased plasma norepinephrine concentration, left ventricular hypertrophy, and dilation were associated with the development of heart failure in this model. Three months after the last embolization, the density and affinity of myocardial beta adrenoceptors and voltage sensitive calcium channels were quantified by analyzing saturation isotherms of specific radioligand binding. [3H]Dihydroalprenolol and [3H]nitrendipine bound specifically and with high affinity to cardiac beta adrenoceptors and calcium channels, respectively. Scatchard transformation of the specific binding of these radioligands in membranes prepared following intracoronary embolization demonstrated a 47% decrease in the density of [3H]dihydroalprenolol binding sites (605 +/- 20 fmol/mg, normal, vs. 323 +/- 18 fmol/mg, failed; P < 0.05) and a 20% decrease in [3H]nitredipine binding sites (371 +/- 11 fmol/mg, normal, vs. 298 +/- 17 fmol/mg, failed; P < 0.05). The binding equilibrium dissociation constants for [3H]dihydroalprenolol and [3H]nitrendipine were not significantly different between normal and failed myocardium. There was no difference in the sialic acid content in the sarcolemmal membranes prepared from normal and failed dog hearts (31.07 +/- 0.76 nmol/mg, normal, vs. 30.58 +/- 5.25 nmol/mg, failed). This is inconsistent with the selective purification of membranes utilized in these radioligand binding studies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial beta adrenoceptor and voltage sensitive calcium channel changes in a canine model of chronic heart failure. 133 65

In experimental models, the characteristics of beta-adrenoceptors in left ventricular hypertrophy (LVH) due to pressure overload remain controversial and no data are still available in man. We investigated right auricular (RA) and left ventricular (LV) beta-adrenoceptors characteristics (125 I cyanopindolol binding) in two groups of patients undergoing valve replacement without heart failure (LV ejection fraction > 55%). Height patients with mitral stenosis (mean age: 64 +/- 4 years) and without LVH (LV mass index < 120 g/m2) constituted the control group and 13 patients with aortic stenosis (mean age: 66 +/- 4 years) and LVH (LV mass index > 150 g/m2) the study group. The results are: [table: see text] These results show that, in man, LVH due to pressure overload does not induce variation of total number beta-adrenoceptors, but is associated with a selective decrease in left ventricular beta 1-adrenoceptors.
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PMID:[Myocardial beta-adrenergic receptors and left ventricular hypertrophy induced by pressure overload in man]. 133 54

A 39-year-old female patient with refractory heart failure has been studied. On February, 1982 she was submitted to right lobar thyroidectomy for remotion of the left thyroid lobe. Following the surgery, she had signs of hypocalcemia and the diagnosis of secondary hypoparathyroidism and heart failure had been made. Seven months after she had acute pulmonary edema, cardiomegaly III (cardiothoracic index = 0.58) with predominant left atrial and left ventricular hypertrophy, which were confirmed by echocardiogram (ECO). The ECO also demonstrated low contractility of the left ventricle. The QT interval was increased on the electrocardiogram (QTc = 0.50 s), the calcium was 5.0 mg/dl with calciuria of 28 mg/day; phosphatemia was 4.8 mg/dl and phosphaturia of 214 mg/day. The level of thyroid hormones (T3 and T4) were in the normal ranges despite the TSH was increased in the beginning of the disease. She was first treated with digitalis, diuretic and vasodilator drugs, thyroid hormone and oral calcium. She had progressive hemodynamic improvement when higher doses of calcium were given with D3 vitamin. The most significant result of this treatment was reduction of the heart size that come back to normal. At the present time patient is treated with thyroid hormone, calcium and D3 vitamin only.
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PMID:[Hypocalcemia causing heart failure]. 134 Jul 40

The major risk factor associated with the appearance of adverse cardiovascular events and outcome attributable to cardiovascular disease is left ventricular hypertrophy (LVH). Why this should be so resides not in the increase in myocardial mass per se, but in the disruption of myocardial structure. An abnormal accumulation of fibrillar collagen within the adventitia of intramyocardial coronary arteries and neighboring interstitial spaces represents such a distortion in structure. Furthermore, this fibrosis disrupts the electrical and mechanical behavior of the hypertrophied myocardium. Mechanisms responsible for fibrillar collagen accumulation have been examined in intact animals and cultured cardiac fibroblasts. In vivo studies indicate that myocardial fibrosis is associated with the presence of chronic mineralocorticoid excess, relative to sodium intake and excretion, not hemodynamic workload. Accordingly, fibrosis can appear in both the hypertensive, hypertrophied and nonhypertensive, nonhypertrophied ventricles. In both primary and secondary hyperaldosteronism it was possible to prevent myocardial fibrosis with an aldosterone receptor antagonist, while in unilateral renal ischemia angiotensin converting enzyme (ACE) inhibition was similarly cardioprotective. A regression in fibrous tissue and normalization of diastolic stiffness has also been possible using ACE inhibition, bringing forward the concept of cardioreparation and the notion that heart failure due to fibrosis may be reversible. In vitro studies indicate that effector hormones of the renin-angiotensin-aldosterone system stimulate fibroblast collagen synthesis. Aldosterone, in pathophysiologic concentrations, and angiotensin II, in much larger concentrations, each enhance collagen synthesis without altering the mitogenic potential of these cells. Thus, elevations in circulating aldosterone and angiotensin II, relative to sodium intake, have the potential to not only alter sodium homeostasis and vascular tonicity, but also the structure of cardiovascular tissue. Thus, myocardial fibrosis represents a structural basis for pathologic hypertrophy and ultimately accounts for the appearance of adverse cardiovascular events and outcomes.
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PMID:Pathologic hypertrophy with fibrosis: the structural basis for myocardial failure. 136 63

In both men and women left ventricular hypertrophy (LVH) is the major risk factor associated with the appearance of diastolic and/or systolic myocardial failure. It is not the growth of cardiac myocytes, however, that is responsible for an abnormal structural remodeling of the hypertrophied myocardium in pathologic LVH, but instead, nonmyocyte cells whose behavior and growth are altered by chronic elevations in circulating hormones. Hormone-mediated cardiac fibroblast proliferation and/or enhanced collagen synthesis, for example, account for myocardial fibrosis. The signals mediating nonmyocyte cell involvement in LVH may also involve locally generated hormones having paracrine properties. Herein we review experimental findings pertaining to the reparative and reactive fibrosis of the myocardium seen in various forms of acquired and genetic arterial hypertension, where circulating or tissue renin-angiotensin-aldosterone systems are respectively activated. These hormonal systems determine whether myocardial structure will be altered in arterial hypertension and, accordingly, if myocardial failure ensues. The mechanisms by which these hormones lead to myocardial fibrosis remain to be elucidated and correspondingly will determine if fibrosis can be effectively prevented. At the same time, experimental strategies that regress excess collagen in LVH have been identified, but need to be developed further to determine if myocardial failure, caused by fibrosis, is indeed reversible in humans.
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PMID:Myocardial fibrosis and the renin-angiotensin-aldosterone system. 138 Jun 19

Left ventricular hypertrophy (LVH) is a well defined cardiovascular risk factor and is frequently detected by echocardiography in hypertensive patients. Systolic cardiac function at rest is usually preserved in hypertension, however, diastolic function may be frequently altered. Evidence for these changes has been demonstrated by Echo-Doppler even without concomitant existence of LVH. Quantitative and qualitative changes in contractile proteins and interstitial tissue as well as reduction of coronary reserve may be related to the mentioned dysfunction. Recent studies have confirmed the precocity of diastolic dysfunction both in laboratory animals as well as man. Further significant differences have been shown between normotensives with and without a family history of systemic hypertension. The relative importance of diastolic disfunction is also related to its possible role in the genesis of cardiac failure and its probable role in the modulation of cardiopulmonary reflexes in addition to the hemodynamics of arterial hypertension. It is not yet known if the presence of diastolic dysfunction is a mechanism or a risk marker like LVH.
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PMID:[Precocity of diastolic dysfunction in hypertensive cardiopathy]. 138 59

The cardiac interstitium is composed of non-myocyte cells and a structural fibrillar protein network which plays a dominant role in governing the structure, architecture, and mechanical behaviour of the myocardium. Herein we review the fibrillar collagen network, its various components, and the functions they serve in the normal and structurally remodelled myocardium in arterial hypertension. The heterogeneity in myocardial structure, created by the altered behaviour of non-myocyte cells, particularly cardiac fibroblasts, which are responsible for collagen synthesis or degradation and thereby fibrous tissue accumulation, is a major determinant for the appearance of diastolic dysfunction and ultimately systolic myocardial failure. Regulatory mechanisms related to this fibrous tissue response are reviewed to draw attention to the hitherto neglected role of cardiac fibroblasts in mediating adverse structural remodelling of the myocardium and showing how this can be prevented through the use of pharmacological agents that interfere with the regulation of the myocardial collagen matrix. Several lines of evidence suggest that circulating and tissue renin-angiotensin-aldosterone systems (RAAS) are involved in the structural remodelling of the non-myocyte compartment. These include the cardioprotective effects of angiotensin converting enzyme (ACE) inhibition and aldosterone receptor antagonism that were found to prevent myocardial fibrosis in the rat with renovascular hypertension. In the rat with genetic hypertension, established left ventricular hypertrophy and abnormal myocardial diastolic stiffness due to interstitial fibrosis, RAAS inhibition resulted in restoration of myocardial structure and function to normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial collagen matrix remodelling in arterial hypertension. 139 56

During the past years, several large trials (Consensus, VHEFT I and II, SOLVD) have shown a significant reduction of mortality in patients with moderate and severe heart failure. However, despite effective treatment with vasodilators, digitalis and diuretics mortality in these patients remains unacceptable high. It seems logic, to state treatment at an earlier stage of the disease to achieve more benefit. The main early pathophysiological disturbance is left ventricular hypertrophy, resulting from hypertension, coronary artery disease, increasing age and obesity. On the long run, LVH may lead to diastolic and systolic heart failure, myocardial ischemia, arrhythmias and sudden death. With ACE-inhibitors LVH can be reduced within 1 month of treatment. The large SAVE- and SOLVD-prevention trials will show, whether this early intervention will improve proposis in patients with asymptomatic heart failure.
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PMID:[Early therapeutic intervention in heart failure]. 141 67

We report the cases of eight children with Marfan syndrome. Seven (87.5%) were diagnosed with cardiopathy, everyone with auscultatory findings. Electrocardiographic patterns were nonspecific. Enlargement of the aortic root was present in two of the cases as seen by thorax x-rays. Echocardiography detected the presence of mitral valve prolapse in 87.5% of the patients (7 cases) and aortic enlargement in 75% of the patients (6 cases). Echocardiography also detected the presence of aortic dysplasia, tricuspid valve prolapse and right and left ventricular hypertrophy. During the follow-up period, no case had cardiac failure. There was no mortality. The aortic enlargement was progressive and was not modified by propranolol treatment. Surgical treatment was not needed. Family history related to this condition was present in a very small percentage (37.5%). We comment on one infantile form of Marfan syndrome with its own phenotype different from that of classical Marfan syndrome.
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PMID:[Marfan syndrome in childhood: cardiovascular manifestations. Echocardiographic changes]. 141 16


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