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

Left ventricular hypertrophy, particularly on the electrocardiogram, is an ominous, not an incidental accompaniment of hypertension and cardiovascular disease. The prevalence of electrocardiographic left ventricular hypertrophy increases with age with a slight male predominance, and one in 10 persons aged 30 to 62 can expect to have it within 12 years. At any age, cardiac enlargement on roentgenograms is twice as prevalent as electrocardiographic left ventricular hypertrophy, and in only 16 percent of those with x-ray evidence of cardiac enlargement does electrocardiographic left ventricular hypertrophy subsequently develop. Hypertension predisposes and at systolic pressures exceeding 180 mm Hg evidence of electrocardiographic left ventricular hypertrophy develops in 50 percent, with no closer relation to diastolic, than to systolic pressure. In addition to drastic curtailment of life expectancy, electrocardiographic left ventricular hypertrophy is a harbinger of serious cardiovascular disease. Definite electrocardiographic left ventricular hypertrophy is associated with an eightfold increase in cardiovascular mortality and a sixfold increase in coronary mortality. Electrocardiographic left ventricular hypertrophy with repolarization criteria more than doubles the risk of hypertension alone and carries a greater risk of cardiovascular morbidity and mortality than cardiac enlargement. It identifies hypertensive patients with a compromised coronary circulation and myocardial damage. Risk of stroke, cardiac failure, and every clinical manifestation of coronary heart disease is substantially increased. In those with electrocardiographic left ventricular hypertrophy risk of cardiac failure is three times that in those with hypertension alone. Electrocardiographic left ventricular hypertrophy based solely on voltage criteria reflects chiefly the severity and duration of associated hypertension, carrying only half the cardiovascular risk of electrocardiographic left ventricular hypertrophy with repolarization abnormality. The precise pathologic and anatomic meaning of electrocardiographic left ventricular hypertrophy is unclear in view of the modest correlations with anatomic, x-ray, ventriculographic, and electrocardiographic measures of cardiac hypertrophy. The electrocardiographic aberrations are as much a product of myocardial damage as hypertrophy, and their appearance must be regarded as a grave prognostic sign in the course of cardiovascular disease.
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PMID:Prevalence and natural history of electrocardiographic left ventricular hypertrophy. 622 93

The cases of 135 consecutive elderly patients 70 years old or older who had valve replacement and related surgical procedures from October, 1977, through April, 1982, were reviewed. There were 75 men and 60 women. The mean left ventricular ejection fraction was 50.16 +/- 5%. The overall operative mortality was 8% (11 patients). The early operative deaths were related mainly to cardiac failure, low cardiac output, sepsis, and renal and multiorgan failure. To assess the operative risk, these 135 patients were compared with 312 younger patients (less than 70 years old) who had undergone similar procedures during the same period. The operative mortality in this group was 5.2% (16). In-hospital complications included arrhythmia (13%), psychosis (7.4%), respiratory failure (6.7%), renal failure (6.7%), cerebrovascular accident (5.2%), myocardial infarction (4.4%), and reoperation for bleeding (2.2%). Wound dehiscence occurred in 1.5% of the patients, and pulmonary emboli and sepsis developed in 0.7%. Of these complications, only the incidence of cerebrovascular accident appeared to be more common in the elderly group (5.2% versus 2.8%), but it had no statistical significance (p = 0.18). A follow-up of 3,892 patient-months was completed in 98.4% of the survivors. There were 8 late deaths (6.4%). Six were related to the valve or to ongoing cardiovascular disease. Thirty-four patients subsequently required medical attention: 4 had bleeding because of the anticoagulant; 3 required a blood transfusion; and 27 were hospitalized. Six were admitted for related cardiac conditions and 7, for observation of other conditions; 14 underwent surgical procedures not related to the cardiovascular system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Should valve replacement and related procedures be performed in elderly patients? 633 51

Sixteen infants, 2 to 35 days of age, had acute renal failure, a diagnosis based on serum creatinine concentrations greater than 1.5 mg/dL for at least 24 hours. Eight infants were oliguric (urine flow less than 1.0 mL/kg/h) whereas the remainder were nonoliguric. To determine clinical parameters useful in prognosis, urine flow rate, duration of anuria, peak serum creatinine, urea (BUN) concentration, and nuclide uptake by scintigraphy were correlated with recovery. Nine infants had acute renal failure secondary to perinatal asphyxia, three had acute renal failure as a result of congenital cardiovascular disease, and four had major renal anomalies. Four oliguric patients died: three of renal failure and one of heart failure. All nonoliguric infants survived with mean follow-up serum creatinine concentration of 0.8 +/- 0.5 (SD) mg/dL whereas that of oliguric survivors was 0.6 +/- 0.3 mg/dL. Peak serum creatinine concentration did not differ between those patients who were dying and those recovering. All infants who were dying remained anuric at least four days and revealed no renal uptake of nuclide. Eleven survivors were anuric three days or less, and renal perfusion was detectable by scintigraphy in each case. However, the remaining survivor (with bilateral renal vein thrombosis) recovered after 15 days of anuria despite nonvisualization of kidneys by scintigraphy. In neonates with ischemic acute renal failure, lack of oliguria and the presence of identifiable renal uptake of nuclide suggest a favorable prognosis.
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PMID:Prognostic factors in neonatal acute renal failure. 646 25

Since the realization that hypertension was a risk factor for cardiovascular disease, methods of lowering elevated blood pressure have been developed. The main goal of antihypertensive treatment is to prevent or to arrest cardiovascular damage. Based on the successes and failures encountered for over 30 years or more of therapeutic experience in hypertension, several treatment goals have been established. Previously, it was claimed that the advantages of lowering blood pressure were not dependent on the antihypertensive drug used. Now, this is being questioned. For instance, fatigue is often observed in hypertensive patients treated with drugs that reduce cardiac output and limit peripheral blood flow. Is it therefore more rational to reduce blood pressure by returning increased vascular resistance to normal? Since antihypertensive therapy is life-long, we are becoming increasingly aware of the long-term effects (both beneficial and adverse) of antihypertensive drugs. The metabolic changes caused by current antihypertensive drugs are now being studied in detail. The potassium-depleting action of diuretics is well-known, and the significance of such an effect is being re-examined. The effects of various antihypertensive agents on serum lipids are relatively recent observations, the clinical importance of which is worthy of wider discussion and investigation. The abolition or reduction of all vascular complications of hypertension is the goal for which current antihypertensive treatment has most often failed. Whereas prevention of cerebrovascular accidents, renal failure, and heart failure has indeed been successfully achieved, coronary complications (the most frequent adjunct of hypertension) have been little influenced by antihypertensive therapy. Is this because coronary heart disease may be simply an associated disease, rather than a consequence of hypertension? Or is this because the beneficial action of the most widely used antihypertensive drugs on vascular disease is largely counteracted by unfavorable metabolic effects? These and similar questions have to be debated and resolved before we can define treatment goals more precisely and develop the most appropriate means to achieve them.
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PMID:Treatment goals in hypertension. 670 59

Prazosin sinks the pathologically increased blood pressure, reduces pre- and afterload in myovascular insufficiency and has an interesting influence on plasma lipid fractions with regard to the coronary risk. Prazosin thus intervenes in the three cardiovascular disease processes, which often exist simultaneously, which are mutually caused. Studies which have taken place in the meantime demonstrate the possibilities of Prazosin as a treatment for Raynaud's disease and gangrene. The relatively long bio-availability of the preparation led constantly to the discovery of additional ranges of application, but did not deliver any new findings which would have made restrictions of the original application necessary. On the contrary, Prazosin proved to be especially favourable and capable of being universally applied in the illnesses which frequently accompany hypertension and cardiac insufficiency.
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PMID:[Hypertensive therapy with prazosin. Concomitant cardiovascular, metabolic and respiratory diseases. Proven facts and potential aspects]. 672 80

In the Framingham Study 2325 men and 2866 women 30 to 62 years old at entry were followed biennially over 22 years for the development of chronic atrial fibrillation in relation to antecedent cardiovascular disease and risk factors. During surveillance, atrial fibrillation developed in 49 men and 49 women. The incidence rose sharply with age but did not differ significantly between the sexes. Overall, there was a 2.0 per cent chance that the disorder would develop in two decades. Atrial fibrillation usually followed the development of overt cardiovascular disease. Only 18 men and 12 women (31 per cent) had chronic atrial fibrillation in the absence of cardiovascular disease. Cardiac failure and rheumatic heart disease were the most powerful predictive precursors, with relative risks in excess of sixfold. Hypertensive cardiovascular disease was the most common antecedent disease, largely because of its frequency in the general population. Among the risk factors for cardiovascular disease, diabetes and electrocardiographic evidence of left ventricular hypertrophy were related to the occurrence of atrial fibrillation. The development of chronic atrial fibrillation was associated with a doubling of overall mortality and of mortality from cardiovascular disease.
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PMID:Epidemiologic features of chronic atrial fibrillation: the Framingham study. 706 92

Hypertension is not simply an acute elevation of arterial pressure during a laboratory experiment. It is the development of a cardiovascular disorder provoking a variety of physiological adaptions brought about by an imbalance of pressor and depressor mechanisms that serve to control arterial pressure at normal levels in the normotensive animal. These pathogenetic mechanisms include hemodynamic, volume, renal parenchymal, sodium, renopressor, catecholamine, neural, hormonal, and even depressor factors. The most common form of the disease is essential hypertension, affecting over 95% of patients with hypertension. Although not the same, the experimental animal model that best mimics essential hypertension is the spontaneously hypertensive rat (SHR). However, to state with certainty that the SHR is a true laboratory duplicate of essential hypertension is inaccurate because the causes of both diseases remain unknown. Both forms are genetically predisposed, naturally occurring, slow but progressive in development, and similar in cardiovascular and hemodynamic adaptions. Both involve arteriolar and venular constriction and myocardial hypertrophy that provide a stable hyperfunctioning adaptation of the heart for a substantial period of time but ultimately lead to cardiac failure, stroke, and other vascular impairment. At best we can conclude that they both represent genetically predisposed disease that involves the disarray of the multifactorial interplay of mechanisms that usually maintain arterial pressure at normal levels.
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PMID:Hemodynamic factors in the pathogenesis and maintenance of hypertension. 708 85

The long term follow up studies on cases of cardiovascular diseases during pregnancy or delivery were reviewed in 181 patients administrated in our clinic. The results as follows: 1. An incidence of patients with cardiovascular disease during pregnancy was 1.46 per cent as a whole, and there was increasing tendency in congenital heart disease. 2. An accidental heart failure during pregnancy was seen in 7.7 per cent and all cases with NYHA III grade had an incidence of 100 per cent. 3. The occurrence of toxicosis and SFD pregnancy were more frequently seen in group of heart disease than in controls. But, no difference was observed in spontaneous abortion or neonatal asphyxia. 4. 28 patients with Starr-Edwards prosthetic heart valves became pregnant in our clinic. In these pregnancies, 5 cases receiving with warfarin therapy resulted in 3 anomalies of new born and in 2 spontaneous abortion. So, the use of warfarin seemed to have the risk to the fetus. But omission of the anticoagulant therapy on the other hand, increased the danger of systemic embolization to the mother. 5. The follow up study by mail in some cases revealed that, as a general, pregnancy and delivery may aggravate the condition of patients, especially who had mitral heart failures.
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PMID:[Clinical studies on cases of cardiovascular disease during pregnancy (author's transl)]. 724 Aug 15

Serial assessment of cardiac function by radionuclide ejection fraction (EF), using a "first-pass" technique, was performed prior to each dose in 292 patients receiving doxorubicin. Detailed analysis was undertaken in 98 patients, consisting of all 91 patients who had received greater than 200 mg/m2 and seven with risk factors (RFs) who had received between 100 and 200 mg/m2. Thirty-two patients had RFs and 66 had no risk factors (NRFs). RFs were: (a) cardiovascular disease, (b) mediastinal irradiation within 6 months of starting doxorubicin treatment, and (c) total doxorubicin dose greater than 550 mg/m2. The criteria for discontinuing doxorubicin were EF less than 0.40 in RF patients or less than 0.35 in NRF patients or decrease in EF of greater than or equal to 0.14 over three successive readings. In the NRF group, no patient met these criteria nor did any develop cardiac failure. In the RF group, discontinuation was indicated in eight patients: two stopped receiving doxorubicin at total doses of 730 mg/m2 and 680 mg/m2, respectively, and it was discontinued in the other six at total doses ranging from 120 to 420 mg/m2. Prior to the first dose of doxorubicin, all patients should have a baseline EF and assessment of RFs. An EF study is required before each subsequent dose in patients with RFs or with initial EF less than 0.45, but in the remaining patients, serial studies are not required until there is a cumulative dose of 450 mg/m2. Use of these guidelines and our criteria for discontinuation may prevent development of doxorubicin cardiotoxicity.
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PMID:Radionuclide ejection fraction in doxorubicin cardiotoxicity. 724 82

A case of timolol-associated heart failure in a 73-year old white man is reported. The patient, with a history of cardiovascular disease and glaucoma, was admitted to the hospital because of complaints of shortness of breath, orthopnea, and reduced exercise tolerance. Chest roentgenogram showed interstitial congestive failure, and an EKG demonstrated sinus bradycardia. The patient's medications before admission included quinidine, isosorbide dinitrate, dipyridamole, aspirin, pilocarpine eyedrops 4%, timolol eyedrops 0.5%, and nitroglycerin ointment and sublingual tablets. On the second day of hospitalization, it was noted that the patient's dyspnea and sinus bradycardia could be related to a recent increase in his timolol dosage. The timolol was discontinued, and the patient's heart rate increased. As the patient's pulse rate increased, the symptoms of congestive heart failure disappeared. This case demonstrated the importance of obtaining complete drug histories from patients. The potential for adverse system reactions resulting from topical medications should be considered.
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PMID:Bradycardia and congestive heart failure associated with ocular timolol maleate. 728 2


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