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

Disorders of the heart frequently cause pulmonary dysfunction because of the close structural and functional association of the heart and lungs. The pulmonary vasculature is very commonly affected by cardiac pathology. The pulmonary vasculature is normally a low-pressure, low-resistance circuit with high compliance and tremendous vascular reserve. Although resting vascular tone is low, there are many identified mediators of pulmonary arterial tone that may help mediate pulmonary blood flow. Alveolar hypoxia is clearly a stimulus for increasing pulmonary vascular resistance although factors that mediate the response to hypoxia are not fully understood. Patients with left-to-right shunting due to congenital heart disease because of elevations in pulmonary artery flow and pressure tend to develop progressive anatomic changes in the pulmonary vasculature. This leads to an increase in pulmonary vascular resistance, irreversible pulmonary hypertension, right heart failure, reversal of shunt flow, and Eisenmenger's syndrome. The degree of anatomic vascular damage due to left-to-right shunting can be graded histologically. Lesser grades of damage are reversible with corrective surgery, whereas more severe grades show no improvement or progression with operation. Chronic left-sided congestive heart failure seen in rheumatic mitral stenosis can cause secondary changes in the pulmonary vasculature. Pulmonary hypertension and increased pulmonary vascular resistance can increase reflexly and form a "second stenosis" that further limits cardiac output. Unlike congenital heart disease, severe grades of pulmonary arterial damage are not seen in left heart failure from mitral stenosis or other causes, and consequently with surgical correction pulmonary hypertension reverses. Pulmonary function testing is adversely affected by congestive heart failure. Both restrictive (stiff lungs) and obstructive (cardiac asthma) defects are observed in congestive heart failure. DLCO is abnormally decreased. With treatment of heart failure these defects reverse. Both elevated systemic and pulmonary venous pressures affect fluid filtration in the pleural space and cause pleural fluid accumulation. The fluid is transudative with low protein, low lactate dehydrogenase, and low cell counts. Transudative effusions from heart failure resolve with treatment. With large effusions and cardiomegaly, pulmonary dysfunction results because of atelectasis from compression and space-occupying effects of the heart and pleural fluid. Following myocardial infarction, cardiac surgery, or other cardiac trauma, the postcardiac injury syndrome can result. The syndrome is characterized by exudative pleural and pericardial effusions along with pulmonary infiltrates, fever, chest pain, leukocytosis, and an elevated ESR. The syndrome must be diagnosed by exclusion of bacterial pneumonia, pulmonary emboli, and congestive heart failure. Treatment is with nonsteroidal anti-inflammatory agents or systemic co
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PMID:Pulmonary and pleural complications of cardiac disease. 268 66

Short-term and long-term use of physician consultations and rehospitalizations were studied in 383 myocardial infarction (MI) patients in relation to demographic, medical, and psychological factors. Short-term (i.e. within 6 months post-MI) utilization of physicians was only related to patients' health locus of control. In comparison, a higher number of physician consultations 3-5 years after the MI was independently related to female sex, more non-cardiac limitations before the MI, more complications during hospitalization, less cardiac lifestyle knowledge, and higher levels of anxiety and depression short time after the MI. Every second patient was readmitted to the hospital before the 3-5 years follow-up but only 14% suffered a non-fatal reinfarction. More rehospitalizations were independently related to a higher number of previous hospitalizations for heart disease, more pre-MI cardiac limitations, less cardiac lifestyle knowledge, and higher initial level of emotional distress. Discriminant analysis identified female sex and patients' initial expectations of reduced emotional control as the best predictor variables for a rehospitalization caused by chest pain without a new infarction, whereas a reinfarction was best discriminated by the number of previous hospitalizations for heart disease. We conclude that psychological factors influence health services utilization to a comparable extent as medical factors. These findings may indicate a greater need for long-term professional support in patients with less initial cognitive and emotional control.
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PMID:Use of health services after a myocardial infarction. 271 Nov 51

A 45-year-old woman with no history of heart disease twice experienced chest pain after consuming a dose of ranitidine. The chest pain, which lasted about one hour, was substernal, left of midline, dull, and pounding. H2-receptors are present in cardiovascular tissues. Although several studies have not noted an effect of ranitidine on cardiac indices there have been case reports indicating a cardiac effect. There are no reports of chest pain associated with H2-blocker ingestion; however, both bradycardia and hypotension (reported effects) might cause chest pain. A discussion of the possible mechanisms is presented.
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PMID:Ranitidine-induced chest pain. 271

In this case report, the hospitalization of a 34-year-old woman with a history of heart disease is described. Arrhythmias and precordial chest pain led to her admission to the coronary care unit. Different therapeutic trials failed. Finally it became obvious that all tachycardias documented by the arrhythmia monitoring system were artifacts, produced by manipulation at the ECG electrodes. After disclosure and confrontation, a psychic misdevelopment in combination with an abuse of analgetics was found.
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PMID:[Simulated tachyarrhythmia. A case report]. 273 91

Many studies indicate that women live longer than men but report more physical illness. This report is the first prospective study of sex ratios for morbidity and mortality due to a variety of causes in a single cohort: a random sample of 5,239 adults, aged 30 years or older in 1965, who have been followed through 1983 (19 years) by cause and age. For both cancer incidence and mortality there was a female excess before age 50 years, followed by a male excess peaking between ages 60 and 69 years. Sex ratios for ischemic heart disease mortality, on the other hand, indicated a male excess at virtually all ages, and that these sex ratios declined with age. However, three measures of heart disease morbidity (self-reported chest pain, heart trouble, and high blood pressure) demonstrated a female excess that did not vary by age. All four measures of functional disability (impaired self-care, impaired mobility, cessation of work, and reduction of work) demonstrated a female excess that did not vary by age (with the exception of a male excess in impaired self-care in adults aged 30 to 39 years). Further analyses of sex differences in health need to acknowledge the heterogeneity of the relation of sex to disease, and the complex age-sex interaction that varies remarkably with both cause and manifestation of outcome (morbidity vs. mortality).
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PMID:Sex differentials in morbidity and mortality risks examined by age and cause in the same cohort. 276 4

Goldsmith and Pilpel found the rate of hospitalization for cardiovascular disease (CVD) in Beer Sheva in 1981 to be approximately twice that of five development towns in the Negev. In order to determine whether this difference was due to differences in the prevalence of heart disease, data on heart disease mortality hospitalization for 1981, 1983 and 1985 was studied, and hypertension prevalence in these communities were examined. From 1981 death records, age-adjusted CVD rates for the male population greater than 30 years were 397.7/100,000 in Beer Sheva and 344.4 in development towns; for women the rates were 351.5 and 411.2, respectively. Myocardial infarction rates for men were the only subset of CVD to be significantly different (Beer Sheva 174.3 vs. development towns 115.7). Beer Sheva residents with CVD were significantly more likely to die in the hospital or another health care facility than residents of development towns. The rates of emergency room use were higher in Beer Sheva than in development towns, but the proportion of those patients who came to the emergency room because of chest pain who were hospitalized was the same for both communities. Data from a sample study of hypertension recorded for patients in primary care clinics in 1983 showed no differences in prevalence or treatment status between Beer Sheva and development town residents. Overall CVD hospitalization rates were 27.7% greater for BS men and 33.3% for BS women. We conclude that: a) the higher rate for myocardial infarction in Beer Sheva merits further investigation, but cannot account for the differential rates of hospital use; and b) distance from the hospital and c) culturally associated attitudes toward hospitalization on the part of both patients and physicians are likely explanations that should be further investigated.
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PMID:Cardiovascular disease hospitalization rates in Negev communities: are differences due to differential prevalence or differential use of health care? 278 52

We have used a sensitive direct radioimmunoassay to study the effects of exercise on plasma atrial natriuretic peptide (ANP) concentrations in man. Plasma ANP concentration increased three-fold in sixteen patients undergoing bicycle ergometer electrocardiographic tests for the investigation of chest pain. Resting ANP concentrations were higher in those patients in whom there was more evidence of heart disease, such as a positive exercise test, treatment with a beta blocker or history of myocardial infarction, although exercise resulted in increased ANP in both groups. We also confirm the increased plasma ANP concentration observed in patients with congestive cardiac failure and renal failure. In nine patients with renal failure routine haemodialysis was accompanied by a 30 per cent reduction in plasma ANP concentration. Plasma ANP concentrations were similar in treated hypertensive patients, untreated borderline hypertensive patients and normotensive subjects.
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PMID:Direct radioimmunoassay of human plasma atrial natriuretic peptide in various normal and pathophysiological states: increase in renal and cardiac failure during exercise. 295 25

To characterize the changes in indications for coronary angiography we compared indications and therapeutic conclusions of cardiac catheterization, including coronary angiography, in 100 consecutive patients in 1975 and 100 consecutive patients in 1985. The baseline characteristics of the patients in the two groups were similar, except for age (50 +/- 10 vs 56 +/- 9 years, p less than 0.0001) and prior angioplasty (0 vs 12, p less than 0.0001). The main indications for coronary angiography in the two groups were (1975 vs 1985) chest pain in 67 vs 62 (n.s.), myocardial infarction in 10 vs 17 (n.s.), prior coronary surgery in 3 vs 0 (n.s.), major arrhythmias in 1 vs 1 (n.s.), and incidental (coronary pathology not the primary issue) in 19 vs 8 (p less than 0.05). We further analyzed each of the main indications in the two groups. Chest pain: angina ruled out in 21% vs 26% (n.s.), stable angina 64% vs 61% (n.s.), unstable angina 15% vs 13% (n.s.), positive non-invasive tests 39% vs 44% (n.s.). Myocardial infarction: acute intervention 0 vs 12% (n.s.), angina after infarction 20% vs 47% (n.s.), positive non-invasive tests after myocardial infarction 20% vs 41% (n.s.). Incidental: valvular heart disease 57% vs 63% (n.s.), cardiomyopathy 26% vs 13% (n.s.), congenital heart disease 11% vs 0 (n.s.), aortic dissection 5% vs 25% (n.s.), other 5% vs 0 (n.s.). Overall, clinical suspicion of coronary artery disease was confirmed and documented in 80% (65/81) vs 77% (61/79) of patients (n.s.), and normal coronary arteries were found in 20% (16/81) vs 23% (18/79) of patients respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Change in indications for coronary angiography in a decade]. 296 11

Intracoronary injection of acetylcholine has been shown to induce coronary spasm in patients with variant angina. To examine its sensitivity and specificity, incremental doses of acetylcholine (20, 50 and 100 micrograms into the left coronary artery and 20 and 50 micrograms into the right coronary artery) were injected into the coronary artery or arteries in 70 patients with variant angina (Group 1) (mean age 57 years) and 93 patients without variant angina or angina at rest (Group 2) (mean age 54 years). Forty patients of the latter group had atypical chest pain, 16 cardiomyopathy, 14 arrhythmia, 11 valvular disease, 7 stable effort angina due to advanced coronary artery disease, 3 congenital heart disease and 2 hypertension. A temporary cardiac pacemaker set at 40 to 50 beats/min was positioned in the right ventricle. Coronary spasm was defined as total occlusion or severe vasoconstriction associated with chest pain or ischemic ST changes on the electrocardiogram or both. In Group 1, acetylcholine induced spasm in 63 (90%) of the 70 patients in the artery or arteries predicted to be responsible for spontaneous attacks. In Group 2, acetylcholine induced coronary spasm only in one patient with effort angina and advanced coronary artery disease although lesser degrees of vasoconstriction (less than or equal to 75% of the luminal diameter) occurred in most patients after acetylcholine (specificity of acetylcholine thus was 99%). In conclusion, intracoronary injection of acetylcholine is sensitive and reliable for the induction of coronary spasm.
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PMID:Sensitivity and specificity of intracoronary injection of acetylcholine for the induction of coronary artery spasm. 304 96

Although patients with angiographically normal coronary arteries have low mortality, several studies have indicated that their social and work morbidity is high. Panic disorder appears to be a major contributor to the continuing chest pain in this population. There are also many chest pain patients appearing in cardiology clinics who also do not have heart disease but who are not given the opportunity to be evaluated for psychiatric disorders. Among those presenting with atypical or nonanginal chest pain, panic disorder represents a likely etiologic consideration. The fact that such patients do exist in cardiology populations is further substantiated by an open-label trial of alprazolam which demonstrated a positive effect in patients selected from those with atypical chest pain and no heart disease found to fit panic disorder criteria. These findings strongly support the increasing affiliation between cardiology and psychiatry and reinforce the belief that many problems of the heart may be problems of the mind/brain.
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PMID:Panic disorder, cardiology patients, and atypical chest pain. 304 7


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