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

Mitral valve prolapse is a common cardiac disorder that can readily be diagnosed by characteristic auscultatory and echocardiographic criteria. Although many diseases have been associated with mitral valve prolapse, most affected individuals have the primary form of the disorder. Mitral valve prolapse is an inherited condition commonly associated with myxomatous degeneration of the mitral valve and its support structures. Complications of mitral valve prolapse, including cardiac arrhythmias, sudden death, infective endocarditis, severe mitral regurgitation (with or without chordae tendineae rupture), and cerebral ischemic events, occur infrequently considering the wide prevalence of the disorder. Panic disorder is a specific type of anxiety disorder characterized by at least three panic attacks within a 3-week period or one panic attack followed by fear of subsequent panic attacks for at least 1 month. It too is a common condition with a prevalence and age and gender distribution similar to that of mitral valve prolapse. Panic disorder and mitral valve prolapse share many nonspecific symptoms, including chest pain or discomfort, palpitations, dyspnea, effort intolerance, and pre-syncope. Chest pain is the symptom in both conditions that most commonly brings the patient to medical attention. The clinical description of chest pain in patients with mitral valve prolapse is highly variable, possibly reflecting multiple etiologies. Chest pain in panic disorder is usually characterized as atypical angina pectoris and as such bears resemblance to the chest pain commonly described by patients with mitral valve prolapse. Multiple investigative attempts to elucidate the mechanism of chest pain in both conditions have failed to identify a unifying cause. Review of the literature leaves little doubt that mitral valve prolapse and panic disorder frequently co-occur. Given the similarities in their symptomatology, a high rate of co-occurrence is, in fact, entirely predictable. There is, however, no convincing evidence of a cause-effect relationship between the two disorders, nor has a single pathophysiologic or biochemical mechanism been identified that unites these two common conditions. Until specific biologic markers for these disorders are identified, it may be impossible to do so. The lack of a proven cause-and-effect relationship between mitral valve prolapse and panic disorder and the absence of a unifying mechanism do not diminish the clinical significance of the high rate of co-occurrence between the two conditions. Primary care physicians and cardiologists frequently encounter patients with mitral valve prolapse and nonspecific symptoms with no discernible objective cause who fail to respond to beta-blockade. Panic disorder should be considered as a possible explanation for symptoms in such patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mitral valve prolapse, panic disorder, and chest pain. 189 9

Previous reports have found an association between coronary vasospasm and migraine. It has been speculated that migraine and variant angina might be manifestations of a generalized vasospastic disorder. To investigate this hypothesis, 74 patients with frequent attacks of migraine were studied using 24-h continuous ambulatory electrocardiography to identify the presence of coronary vasospasm. Control groups consisted of 19 patients with tension headaches, and 38 healthy individuals. All subjects were free of heart disease. One patient in the migraine group and one patient in the control group had symptomless episodes of ST-segment depression not indicative of coronary vasospasm. Our data do not support the hypothesis that migraine and variant angina are components of a generalized vasospastic disorder.
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PMID:Lack of association of migraine with coronary vasospasm. 194 Jul 82

Twenty-three consecutive subjects (age 46.7 +/- 21, range 13-78) addressed to our attention for symptoms attributed to documented or suspected supra ventricular arrhythmias underwent transesophageal electrophysiologic study. On the basis of the preliminary investigations 15 proved free from organic heart disease, 2 were affected with ischemic heart disease (secondary angina), 6 with hypertensive cardiomyopathy. In each patient the sensibility, specificity and positive predictive value of the following reports regarding the occurrence of paroxysmal fibrillation and flutter (Ffap) were evaluated: a) echo reports of left atrial enlargement; b) ECG signs of atrial enlargement; c) interatrial conduction time (TCIA) assessed with unipolar transesophageal recording. As TCIA we adopted the time interval intercurrent from the first low-voltage deflection of the esophageal P wave (far field) and the apex of the intrinsecoid deflection of the same wave. TCIA proved significantly longer in the 12 patients affected with Ffap compared with those free from documented paroxysmal or inducible arrhythmias or affected with paroxysmal junctional reciprocating tachycardias: 76.6 +/- 11 vs 51.8 +/- 11.7; p less than 0.001. A TCIA greater than 63 msec characterizes with satisfactory sensibility and specificity the occurrence of Ffap: sens. 75%, spec. 91%, positive predictive value 90%. Echo and ECG reports of atrial enlargement behave as highly specific but not sufficiently sensitive indexes of the occurrence of Ffap: sens. 42%, spec. 100%, pos. pred. val. 100% and sens. 17%, spec. 100%, pos.pred.val. 100% resp. We concluded that TCIA is an index correlated with and predictive of the occurrence of Ffap in patients symptomatic for cardiopalmus or neurologic symptoms in the absence of other arrhythmias detectable with Holter monitoring which are able to produce clinical symptoms.
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PMID:[Estimation using unipolar transesophageal recording of the interatrial conduction time in patients with paroxysmal atrial flutter and fibrillation]. 196 40

The Caerphilly Collaborative Heart Disease Study is based on a large cohort of men (2,398) aged 49-66 years at the time of study. Platelet aggregation induced by collagen, thrombin, and ADP was measured in fasting blood samples and was related to prevalent angina, past myocardial infarction, and electrocardiographic evidence of ischemic heart disease. A number of subjects had taken aspirin, other nonsteroidal anti-inflammatory drugs, or other drugs affecting platelet aggregation 7 days before blood sample collection; after the exclusion of these subjects, data were available for 1,811 men. No relations were demonstrated with angina, but significant relations were shown between past myocardial infarctions and electrocardiographic evidence of ischemia and ADP-induced aggregation (both primary and secondary) and between electrocardiographic evidence of ischemia and thrombin-induced aggregation. The strongest relation indicated more than a twofold increase in the odds of a past myocardial infarction in subjects of the highest fifth of ADP-induced primary platelet aggregation compared with the lowest fifth. No significant relations were detected with collagen-induced aggregation. Accounting for a number of possible confounding factors had a relatively small impact on the relations between platelet aggregation and ischemic heart disease. Other evidence, including the well-established effect of aspirin on reducing the incidence of ischemic heart disease, indicates that the relations we describe are unlikely to be simply an effect of IHD on platelets.
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PMID:Ischemic heart disease and platelet aggregation. The Caerphilly Collaborative Heart Disease Study. 198 96

The prevalence of esophageal chest pain was studied prospectively in patients referred on an elective basis to a cardiac unit for suspected myocardial ischemia. A group of 248 consecutive patients without previously documented heart disease was admitted for elective diagnostic coronary angiography. The clinical history classified 185 patients as having anginal pain and the coronary angiogram was normal in 48 of them. In 37 of these 48 patients full esophageal testing was performed including 24-hr intraesophageal pH and pressure recordings with indication of chest pain episodes as well as a number of esophageal provocation tests, ie, acid perfusion, edrophonium stimulation, balloon distension, and ergonovine stimulation, all performed under continuous esophageal manometric and electrocardiographic monitoring. In 19 of these 37 patients, the familiar chest pain could be reproduced by esophageal provocative testing without ischemic ST-T segment alterations; six of these 19 patients had also a positive 24-hr pH and pressure recording. These data strongly suggest an esophageal origin of chest pain in half the patients with typical angina and a normal coronary angiogram.
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PMID:Prospective study on prevalence of esophageal chest pain in patients referred on an elective basis to a cardiac unit for suspected myocardial ischemia. 198 69

The ten-year coronary heart disease (CHD) mortality is reported for 18,322 male civil servants aged 40 to 64 according to questionnaire responses at entry into the Whitehall study. In all 1714 died, 723 from CHD. The predictive power of the questionnaire was examined with a view to its use as a screening tool in population studies. In predicting death from coronary heart disease the greatest specificity (true negative rate) was achieved with men reporting both angina (A) and a history of severe chest pain (possible myocardial infarction, PMI). This strategy (A plus PMI) achieved a specificity of 99% but a sensitivity (true positive rate) of only 7%. In contrast, in men reporting angina and/or PMI, specificity was 90% and sensitivity 29%. If this 'and/or' algorithm was extended to include the report of dyspnoea, diabetes, and/or attending a primary care physician with heart disease or hypertension, then specificity was still 85%, but sensitivity increased to 44%. This combination (11 questions in all) is therefore recommended for screening purposes. Identifying and excluding those who favour positive answers ('yes-set' responders), using questions such as the effect of weather on breathing, led to small increases in specificity but relatively large falls in sensitivity. Among subjects reporting chest pain, those who also complained of non-specific symptoms experienced only half the mortality of those with none of these additional complaints.
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PMID:Predicting death from coronary heart disease using a questionnaire. 208 19

Despite the fact that numerous studies have been published regarding the possible presence in plasma of an endogenous Na-K pump inhibitor with a digitalis-like structure in essential hypertension, very little is known about this factor in heart disease in general, and in situations characterized by low cardiac output. We measured the ability of plasma obtained from the femoral vein to inhibit a human renal Na(+)-K+ ATPase before and immediately after percutaneous transluminal coronary angioplasty (PTCA) in 6 patients suffering from angina pectoris and severe coronary stenosis. Intraerythrocyte sodium and potassium concentrations were also measured simultaneously. Na(+)-K+ ATPase inhibition proved significantly greater after angioplasty as compared to basal activity (percentage inhibition: 31.5 +/- 7.8 vs 16.1 +/- 12.2). No significant changes in intraerythrocyte sodium and potassium were detected. Though we are not in a position to define the mechanism underlying the increase in the digitalis-like factor, a plausible hypothesis may be that the reduction in cardiac output during PTCA by raising cardiac pressures may stimulate the production of a factor of compensatory inotropic significance.
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PMID:Increase in plasma digitalis-like activity during percutaneous transluminal coronary angioplasty in patients with coronary stenosis. 216 10

The effects of Ticlopidine on platelet function at rest and after exercise test in 12 patients with a history of myocardial infarction but no risk factors and/or residual angina, were investigated. The patients were treated with 500 mg per diem Ticlopidine or placebo for 15 days in a crossover double-blind study. Blood samples were taken before and 3 minutes after maximum effort exercise cycle tests. Blood samples from 25 healthy volunteers of comparable age and sex were used for control purposes. The parameters examined were: platelet aggregation induced by ADP (1 and 3 mumol/l), Arachidonic Acid (AA) (1.3 mmol/l) and collagen (2 micrograms/ml); the presence of circulating platelet aggregates and plasmatic fibrinogen levels. When compared with the controls, the patients showed higher levels of aggregation caused by ADP, AA and collagen as well as circulating aggregates. Exercise produced a statistically significant increase in platelet activation, while Ticlopidine significantly inhibited the platelet aggregation induced by ADP, AA and collagen as well as circulating aggregates both at rest and after the exercise test. Fibrinogen levels were higher in the heart attack patients than the controls especially after exercise, but not to a statistically significant degree. Treatment with Ticlopidine did not influence plasma fibrinogen levels. It is not known whether the patients with signs of effort-induced platelet aggregation run a higher risk of ischaemic cardiopathy or whether drug treatment could prevent this eventuality.
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PMID:[Effects of ticlopidine on platelet function at rest and after exercise in patients with previous myocardial infarct. An acute crossover double-blind study]. 217 69

This paper reviews current evidence from several cardiology populations that suggests panic disorder is prevalent and underdiagnosed. Cardiology patients with atypical angina and no heart disease have a high likelihood of having panic disorder as suggested by studies of two separate cardiology populations. That they resemble psychiatric populations with panic is suggested by their positive response to alprazolam. Although evidence is less clear concerning the relationship between MVP and panic, it appears that patients referred to ECHO and found to have MVP are also likely to have panic. Three other populations deserving further study are patients with 1) pacemaker syndrome, 2) coronary artery disease with atypical angina and 3) certain arrhythmias.
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PMID:Panic disorder in cardiology patients. 218 3

Silent myocardial ischaemia can be defined as the presence of transient ischaemic alterations in absence of angina. Those include metabolic, functional, electrocardiographic and anatomic abnormalities without typical chest pain. Its incidence, prognostic significance, possible identification in clinical practice as well as need for treatment varies according to the group of patients. In the present review, we discuss these concepts in base of the knowledge supported by the results of different studies. As a rule, the incidence, prognostic significance, and henceforth the need for its identification, increase from the low risk groups of patients to those of high risk according to classical criteria. To this respect, it is useful to differentiate three groups of patients: normal subjects, stable coronary heart disease and unstable heart disease. Medical treatment with anti-ischaemic drugs as well as myocardium revascularization procedures have shown to decrease the incidence and severity of silent myocardial ischaemia, but its influence on prognosis is unknown, and it should be emphasized that the main objective in the treatment of silent ischaemia is improve prognosis.
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PMID:[Silent ischemia. To treat or not to treat?]. 218 63


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