Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vascular spasm has been considered to be an important component of the eclamptic state. If this abnormal vascular reactivity affects the coronary arteries in eclampsia, one might expect to find areas of myocardial contraction band necrosis, a lesion secondary to coronary reflow after periods of no flow. We reviewed the cardiac findings in the 34 patients with fatal eclampsia (hypertension, edema, proteinuria, and convulsions without evident cause) autopsied at The Johns Hopkins Hospital since 1899, and compared each with the next pregnant or puerperal nontoxemic autopsied patient. The eclamptic patients were 15-45 years old (average 27 years). Convulsions began antepartum in 21 patients, intrapartum in eight, and postpartum in five. The hearts weighed 200-407 g (average 312 g). One heart had rheumatic valvular disease and one had myocarditis. Histologic study of heart sections showed the presence of contraction band necrosis in 12 cases (35%). The control cases included two patients with rheumatic valvular disease, two with endocarditis, two with myocarditis, two with pericarditis, and one with leukemic infiltration. Only one control patient (3%) had contraction band necrosis (p less than 0.001). The frequent occurrence of myocardial contraction band necrosis suggests that coronary artery spasm may be common in patients who die with eclampsia.
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PMID:Morphologic evidence for coronary artery spasm in eclampsia. 719 18

The basic disorder in sinoatrial disease is a functional and/or anatomical defect in the sinus node and the atrium respectively. The clinical feature includes palpitations, angina pectoris, heart failure, giddiness and systemic emboli. Associated diseases are coronary heart disease, hypertension, diphtheria, myocarditis or rheumatic fever. Diagnosis is primarily made by clinical symptoms and conventional or long term ECG-monitoring. However, impaired sinus node function including sinusbradycardia, sinus arrest, sinoatrial block and the bradycardia-tachycardia syndrome cannot easily be assessed, when rhythm disturbances are occurring intermittently, as the recording of electrical activity of sinus node pacemaker cells is not available in man. Therefore methods of provocative atrial stimulation (rapid atrial stimulation, premature atrial stimulation) have been developed for (indirect) estimation of sinus node recovery time and sinoatrial conduction time. Treatment depends on symptoms. In most cases implantation of an electric pacemaker is mandatory since drug treatment usually is unsatisfactory. The natural history of the sinoatrial disease is imperfectly known but probably covers 5--10 years.
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PMID:[The sick sinus syndrome. What causes it?]. 722 53

The conductive system of the heart was studied morphometrically in serial sections in 12 autopsy observations of sudden cardiac death. In 11 cases the sudden death was due to chronic ischemic disease of the heart, in 1 case to idiopathic myocarditis of Abramov-Fidler. The control consisted of 12 autopsy observations of subjects dying of mechanical trauma, alcoholic toxicity, cerebral hemorrhage in the presence of hypertension. In 4 out of 12 observations of sudden cardiac death, acute dyscirculatory disorders of the microcirculatory bed and focal destructive changes of specific muscle fibers were detected in the conductive system of the heart. The intensity of atrophic and sclerotic processes in ganglions of the conductive system was not significantly different from that in the controls.
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PMID:[Changes in the heart conduction system in sudden cardiac death]. 723 27

A retrospective study of 112 cases of lupus erythematosus, 103 acute disseminated lupus erythematosus (ADLE) and 9 chronic discoid lupus (CDL), was conducted to determine the incidence of disorders of conduction (DC), and to study their prognosis and discuss their pathogenicity. The mean age of the group was 38 +/- 16 years, and the mean follow-up period after discovery of the DC was 53 months. Cardiac lesions were present in 49.5 p. cent of the 103 patients with ADLE : pericarditis in 27 p. cent, murmur from lupus endocarditis or cardiomyopathy in 23 p. cent, heart failure in 4.8 p. cent, and hypertension in 17 p. cent. Disorders of conduction were present in 18 (17.5 p. cent) of the 112 patients studied. These included 5 partial right bundle-branch blocks (no complete right bundle-branch block), 2 complete and 3 partial left bundle-branch blocks, 5 complete, 2 first degree, and 1 second degree atrioventricular blocks (AVB). The atrioventricular blocks were usually located in the truncal or fascicular regions, but in 2 cases they were nodal in origin. The 5 complete AVB were associated with ADLE in two cases and CDL in the three other cases. The AVB in the ADLE cases appeared 9 to 20 years after the onset of the lupus, these two patients developing pericardiomyocarditis unaccompanied by disorders of conduction. The three complete AVB occurring during CDL were detected 9 to 18 months after the diagnosis. A fatal outcome was noted in 13 (12.5 p. cent) of the ADLE patients and one of the 9 cases of CDL. Ten-year survival curves showed no difference in prognosis for the groups with or without disorders of conduction, but mortality increased in patients with DC after 10 years. As disorders of conduction were more frequently observed in patients with lupus than in a control population, they can be attributed to either a lupus myocarditis or prolonged administration of synthetic antimalarial agents. Disorders of conduction, and particularly complete AVB are, in fact, observed in patients without pericardiomyocardial lesions, and when they exist usually develop a long time after the onset of the cardiac lesion. All patients had been treated with antimalarials, however, and the onset of the DC was associated with a chloroquine myopathy in some of them. Three of the five complete AVB were observed during the course of CDL in patients without cardiac lesions, this being a supplementary argument for implicating synthetic antimalarials.
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PMID:[Disorders of conduction in lupus erythematosus : frequency and incidence in a group of 112 patients (author's transl)]. 730 72

The decade from 1982 through 1992 witnessed tremendous growth in pediatric cardiac transplantation. At Children's Hospital of Pittsburgh 66 cardiac transplants were performed during this period (age range 7 hours to 18 years). The cause of cardiomyopathy was congenital (n = 30), cardiomyopathy (n = 29), myocarditis (n = 2), doxorubicin toxicity (n = 2), ischemic (n = 1), valvular (n = 1), and cardiac angiosarcoma (n = 1). Nine children (14%) required mechanical circulatory support before transplantation: extracorporeal membrane oxygenation (n = 8) and Novacor left ventricular assist system (n = 1) (Baxter Healthcare Corp., Novacor Div., Oakland, Calif.). The mean follow-up time was 2 years (range 4 months to 8 years). The overall survival in the group was 67%. In children with congenital heart disease (> 6 months of age) the perioperative (30 day) mortality was 66% before mid-1988 (n = 10) and 0% since mid-1988 (n = 11). The late mortality (> 30 days) in children with cardiomyopathy transplanted prior to mid-1988 was 66% (n = 14) and 7% since mid-1988 (n = 15). Since mid-1988 1- and 3-year survival was 82% in children with congenital heart disease and 90% in children with cardiomyopathy. Twenty-six children have had FK 506 as their primary immunosuppressive therapy since November 1989. Survival in this group was 82% at 1 and 3 years. The actuarial freedom from grade 3A rejection in the FK group was 60% at 3 and 6 months after transplantation versus 20% and 12%, respectively, in the 15 children operated on before the advent of FK 506, who were treated with cyclosporine-based triple-drug therapy (p < 0.001, Mantel-Cox and Breslow). Twenty of 24 children (83%) in the FK 506 group are receiving no steroids. The prevalence of posttransplantation hypertension was 4% in the FK 506 group versus 70% in the cyclosporine group (p < 0.001, Fisher). Renal toxicity in children treated with FK 506 has been mild. Additionally, eight children have been switched to FK 506 because of refractory rejection and drug toxicity. FK 506 has not produced hirsutism, gingival hyperplasia, or abnormal facial bone growth. The absence of these debilitating side effects, together with the observed immune advantage and steroid-sparing effects of FK 506, hold tremendous promise for the young patient facing cardiac transplantation and a future wedded to immunosuppression.
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PMID:A decade (1982 to 1992) of pediatric cardiac transplantation and the impact of FK 506 immunosuppression. 768 Mar 96

Autopsy data of 58 cases (1958-1986) was analysed for cardiac lesions. The cases were divided into 2 groups; paediatric (23) and adult (35). The heart was normal in 8.7% and 20.5% of the above groups respectively. Rest of the cases showed left ventricular hypertrophy with variable dilatation. Obstructive lesion in the aorta and or renal arteries was present in 91.3% of paediatric and 80.0% of adult cases. Congestive cardiac failure was very common in paediatric group (60.8%) and was not seen in absence of obstructive lesion in the aorta or renal arteries. Histologically the aortic lesion was healed in 70% and 50% of paediatric and adult cases. The commonest additional lesion found, was coronary artery involvement in 11 cases (17%). Ostial stenosis was noted in 7 cases, including 2 in paediatric age group. Epicardial coronaries were involved in 4 cases with infarcts in 4. Aortic incompetence was rare (3.4%). Associated rheumatic mitral stenosis was seen in 2 and healed infective endocarditis in one. Histologically apart from the above mentioned lesions the myocardium showed essentially a response to hypertension. Focal lymphocytic infiltration was seen in 2 children and tuberculosis myocarditis in 3 adults. No case of any other type of myocarditics or cardiomyopathy was seen. In conclusion hypertension and coronary artery disease are the main factors responsible for myocardial failure but additional related or unrelated factors were present in 15.0% cases.
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PMID:Cardiac lesions in non-specific aorto-arteritis. An autopsy study. 798 78

To elucidate the incidence and clinical significance of ventricular late potentials (LP) and reduced heart rate variability (HRV) in primary and secondary heart muscle disease, 157 patients with dilated cardiomyopathy (DCM, n = 19), chronic myocarditis (MC, n = 50), hypertrophic cardiomyopathy (HCM, n = 27) and systemic hypertension (HT, n = 61) were studied. LP measured by the signal averaging technique were found in 24% of the total study group--47% of the patients with DCM, 28% with MC, 29% with HCM and 10% with HT. Complex ventricular arrhythmias were detected during Holter monitoring in 56% of patients with DCM, in 41% with MC, in 21% with HT and in 16% with HCM. An electrophysiological study was performed in a total of 75 patients. Non-sustained or sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) were inducible during programmed ventricular stimulation in 32% of patients with MC, in 30% with HT, in 20% with DCM and in 17% with HCM. The total duration of the signal-averaged, filtered QRS complex was the only independent predictive factor for severe arrhythmic events and sudden cardiac death. HRV measured in 39 patients were most reduced in patients with DCM (RR interval standard deviation (HRV-SD) 39 +/- 23 ms), followed by 44 +/- 16 ms in patients with HCM, 45 +/- 28 ms in patients with HCM and 67 +/- 51 ms in patients with HT. A significant reduction in the HRV-SD below 30 ms was recorded in 24% of patients measured.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Late potentials and heart rate variability in heart muscle disease. 799 67

The peripartum cardiomyopathy is a rare condition in Europe but a very frequent disease in Sahelian Africa. The risk factors are: heat, hard physical exertion during pregnancy, hypertension, sodium diet, ablutions with hot water during the postpartum period, selenium deficiency and probably latent myocarditis (viral?)
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PMID:[Peripartum dilated cardiomyopathy. A model of multifactor disease?]. 800 29

The main pathologic findings in 23 patients with acquired immunodeficiency syndrome (AIDS) and Chagas' disease are reviewed; five are from our own experience and 18 from the literature. The presence of Trypanosoma cruzi parasites and/or T. cruzi antibodies in blood and cerebrospinal fluid was recorded and computerized tomograms of the brain were evaluated. Twenty (87%) of the 23 subjects developed severe, multifocal or diffuse meningoencephalitis with necrosis and hemorrhage associated with numerous tissue parasites. The second most severely affected site was the heart. Seven (30.4%) of the 23 cases had myocarditis on pathologic examination. It was acute in four patients, chronic in two, and simultaneously acute and chronic in one. Acute myocarditis and meningoencephalitis are interpreted as being caused by relapses of chronic T. cruzi infections. An AIDS permissive role is suggested for these conditions since immunologic defense against T. cruzi is mediated mainly by T lymphocytes, whose CD4 subpopulation is depleted in patients with this disease. Consequently, AIDS is a factor that may favor the reactivation of T. cruzi infections. The lesions reported in the association of Chagas' disease with AIDS were compared with those reported from patients without AIDS having fatal, acute, vector-transmitted infections, contaminated blood transfusions, or accidental exposures in the laboratory. For the latter three, meningoencephalitis is uncommon. Only immunosuppressed cases of Chagas' disease have been described as having a pseudotumoral presentation that shows expanding lesions with a mass effect in the cranial cavity that causes intracranial hypertension and simulates neoplasms (tumors such as gliomas, lymphomas, metastases, etc.).
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PMID:Pathology of patients with Chagas' disease and acquired immunodeficiency syndrome. 814 85

This study was designed to evaluate whether myocardial risk factors other than those strictly related to human immunodeficiency virus infection contribute to histologic cardiomyopathic changes in acquired immunodeficiency syndrome patients. We analyzed 91 consecutive adult human immunodeficiency virus-positive autopsy cases (85% acquired immunodeficiency syndrome by Centers of Disease Control criteria) from 1987-1991 for histologic cardiomyopathic changes (e.g. myocyte hypertrophy and myocardial fibrosis). We correlated the presence of cardiomyopathy with the following common myocardial risk factors: hypertension, coronary artery disease, alcoholism, diabetes mellitus, and valve disease. Forty percent of all cases had cardiomyopathy. Hypertension and coronary artery disease were both more common in the cardiomyopathy group (P < 0.05), compared with those human immunodeficiency virus-positive cases without cardiomyopathy. The other myocardial risk factors did not differ significantly between the two groups when compared individually, but when these data were pooled, 67% of cardiomyopathic patients had one or more myocardial risk factors versus 45% in the noncardiomyopathic group (P < 0.05). Cardiomyopathic patients were also more likely to have multiple myocardial risk factors (P < 0.05). Nineteen percent of cardiomyopathic patients had myocarditis versus 11% in the noncardiomyopathic group (P = NS). Patient age, gender, risk factors for human immunodeficiency virus infection (71% intravenous drugs), and history or autopsy findings of viral infection (e.g. cytomegalovirus) did not differ significantly between the two groups. In our patient population, which is heavily weighted towards intravenous drug use, myocardial risk factors other than human immunodeficiency virus are common, and appear to be major contributors to histologic cardiomyopathic changes that might otherwise be attributed to human immunodeficiency virus infection alone.
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PMID:Myocardial risk factors other than human immunodeficiency virus infection may contribute to histologic cardiomyopathic changes in acquired immune deficiency syndrome. 824 12


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