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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy. A 64-year-old woman was admitted because of dyspnea. There was no past history of hypertension or heart disease and no family history of hypertrophic cardiomyopathy. Laboratory examinations revealed general inflammatory changes and mild elevation of serum CK and GOT. The clinical course was fulminant and the patient died of heart failure one day after admission. On autopsy, asymmetric septal hypertrophy was revealed and the pathohistological examination revealed panmyocarditis with mononuclear cell infiltration, interstitial edema, necrosis of myocytes, and giant cells. The inflammatory changes were most severe in the ventricular septum with asymmetric septal hypertrophy. The extent of myocardial fibers with disarray was within normal limits. Thus, the asymmetric septal hypertrophy appeared to be due to marked interstitial edema and inflammatory cell infiltration in the septum. This case suggests that myocardial inflammation and edema may cause thickening of the ventricular wall during the course of acute myocarditis.
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PMID:Idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy. 295 39

Stings from scorpions (Buthus tamulus) produce acute myocarditis and can result in death in children and adults. Acute myocarditis was induced in anaesthetised dogs by intravenous injection of 4 mg/kg venom (Buthus tamulus). Myocarditis was confirmed by ECG. Blood was collected before and 30 minutes after venom treatment and processed for osmotic fragility. An increase in osmotic fragility of red cells in addition to initial hypertension followed by hypotension were observed in venom treated animals. These results suggest that scorpion venom causes autonomic storm and the released catecholamines were responsible for acute myocarditis, changes in the blood pressure and increased osmotic fragility of red cells.
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PMID:Increased osmotic fragility of red cells in dogs with acute myocarditis produced by scorpion (Buthus tamulus) venom. 355 11

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

The concept of "cardioprotection" with ACE inhibitors has evolved over the last decade. In the 1980s, protective benefits of ACE inhibitors in hypertension were established, regression of left ventricular hypertrophy was demonstrated, and improved ventricular function and survival in mild-to-moderate and severe congestive heart failure was documented. A further "protective" role of ACE inhibitors in coronary artery disease is emerging as more attention is focused on the concept of local tissue renin-angiotensin systems. Recent contributions to the literature describe significant benefits of ACE-inhibitor therapy in acute myocardial infarction, including suppression of ventricular arrhythmias and reduction of both early and late ventricular dilation, preservation of left ventricular function, and improved survival. All of the above effects can be considered "cardioprotective." However, as new benefits are reported in the 1990s, a broadened view of "cardiovascular protection" emerges from investigative studies in the literature. ACE inhibitors may reduce tolerance to nitrates, reduce angina in some but not all studies, and limit smooth muscle cell proliferation (and perhaps restenosis) induced by experimental balloon angioplasty. Local vascular effects may attenuate atherosclerotic changes in the arterial wall in experimental animals and may decrease the incidence of aneurysm formation in hypertensive animals. The effectiveness of ACE inhibitors in acute myocarditis, suggested by reports that captopril may reduce lesions of murine myocarditis when administered early after infection with coxsackievirus B3, requires clinical confirmation. Despite these apparently diverse "cardiovascular protective" consequences of ACE inhibitor therapy, the mechanism(s) of action of these agents remain to be elucidated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardioprotection with angiotensin-converting enzyme inhibitors: redefined for the 1990s. 843 34

Pheochromocytoma, a relatively rare (0.1-0.8% of hypertensives), catecholamine-secreting tumor, is almost always lethal unless recognised and appropriately treated. Histological changes in myocardium can be often found in patients with hypertension crisis due to pheochromocytoma, however, only a few patients with clinical manifestations of acute myocarditis were described. We report a 18-year-old man hospitalised with symptoms of acute myocarditis. Precise clinical assessment allowed to diagnose pheochromocytoma.
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PMID:[Pheochromocytoma mimicking acute myocarditis]. 1511 61

Ang II (Angiotensin II) has been shown to play a pivotal role in the pathophysiology of various organs, especially the cardiovascular system. The effects of ARBs (Ang II receptor blockers) in the treatment of hypertension, congestive heart failure and myocardial fibrosis have been analysed extensively in human trials, as well as animal models, and the focus of interest is now directed to its pleiotropic effects, especially on inflammatory disorders. To investigate the effects of a new ARB, olmesartan, on immune-mediated myocardial injury, the protective effects of olmesartan on the development of murine acute myocarditis caused by CVB3 (coxsackievirus B3) were analysed. Olmesartan and a non-specific vasodilator hydralazine lowered systolic blood pressure of mice on day 7 after virus inoculation to a similar extent. Olmesartan significantly decreased myocardial inflammation compared with controls, whereas hydralazine significantly increased this. Olmesartan significantly decreased the expression of IFN-gamma (interferon-gamma), FasL (Fas ligand), iNOS (inducible nitric oxide synthase) and PFP (pore-forming protein) in myocardial tissue, indicating that olmesartan suppressed the activation of infiltrating killer lymphocytes. Olmesartan also decreased the expression of CVB3 genomes in myocardial tissue as well as serum levels of 8-OHdG (8-hydroxy-2'-deoxyguanosine), a biomarker of oxidative-stress-induced DNA damage. The findings suggest that olmesartan prevents myocardial damage and may improve the prognosis of patients with acute myocarditis; however, further investigations are needed before clinical use.
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PMID:Effect of the angiotensin II receptor blocker olmesartan on the development of murine acute myocarditis caused by coxsackievirus B3. 1633 7

A 69-year-old man with no remarkable medical history was admitted to the intensive care unit in septic shock due to severe community-acquired pneumonia. Twelve hours later he developed electrocardiographic abnormalities with ST elevation in leads II, III, aVF, V5, and V6 in the absence of chest pain and the presence of dyspnea, agitation, and hypertension. Serial measurements of cardiac enzymes were also elevated. Acute coronary syndrome was suspected. A cardiac ultrasound revealed left ventricular dilation with akinesia and systolic dysfunction (ejection fraction, 40%). Emergency catheterization revealed normal coronary arteries, suggesting a probable diagnosis of acute myocarditis. From the fourth day, the patient was progressing favorably. Findings in a follow-up ultrasound were consistent with the onset of dilated myocardiopathy, and angiotensin converting enzyme inhibitors were prescribed. All serology and microbiological studies were negative. Fifteen days after admission the patient was discharged to home after clinical, radiologic and analytic recovery.
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PMID:[Myocarditis in the differential diagnosis of acute coronary syndrome]. 1682 73

Pheochromocytoma is a rare, catecholamine-secreting tumor. The classic symptoms are headache, diaphoresis, and tachycardia with paroxysmal hypertension. Other less common cardio-vascular manifestations, such as arrhythmias, angina pectoris, acute myocardial infarction, dilated cardiomyopathy, acute heart failure, and cardiogenic shock, have occasionally been reported. Here, we report two middle-aged men with acute myocarditis and cardiogenic shock, who needed an intra-aortic balloon pump and extra-corporeal membrane oxygenation for life support. They were diagnosed with pheochromocytoma and underwent laparoscopic adrenectomy that restored cardiac function. These cases illustrate diagnostic and management considerations in pheochromocytoma complicated by acute myocarditis and cardiogenic shock.
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PMID:Pheochromocytoma presenting as acute myocarditis with cardiogenic shock in two cases. 1907 41

Sport activity is an important issue in many patients with a pacemaker either because they performed sport activities before pacemaker implantation to reduce the cardiovascular risk or to improve the course of an underlying cardiovascular disease (e.g. coronary artery disease, heart failure) by sports. Compared to patients with an implantable cardioverter defibrillator (ICD) the risks from underlying cardiovascular disease (e.g. ischemia, heart failure), arrhythmia, lead dysfunction or inappropriate therapy are less important or absent. Sport is contraindicated in dyspnea at rest, acute heart failure, new complex arrhythmia, acute myocarditis and acute myocardial infarction, valvular disease with indications for intervention and surgery and comorbidities which prevent physical activity. Patients with underlying cardiovascular disease (including hypertension) should preferably perform types and levels of physical activity that are aerobic (with dynamic exercise) such as running, swimming, cycling instead of sport with high anaerobic demands and high muscular workload. In heart failure, studies demonstrated advantages of isometric sport that increases the amount of muscle, thereby preventing cardiac cachexia. Sport with a risk of blows to the chest or physical contact (e.g. boxing, rugby, martial arts) should be avoided. Implantation, programming and follow-up should respect specific precautions to allow optimal physical activity with a pacemaker including implantation of bipolar leads on the side contralateral to the dominant hand, individual programming of the upper sensor and tracking rate and regular exercise testing.
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PMID:[Sport for pacemaker patients]. 2285 24

The incidence of cardiovascular diseases in pregnancy is estimated at about 1%. Pregnant women suffer from rheumatic diseases of the heart valves, hypertension, congenital heart deffects, inflammatory and ischemic disorders or pathologies of the electrical conduction system of the heart. Myocarditis during pregnancy occurs very seldom. Few cases of severe myocarditis during gestation have been reported in the literature. This report presents a case of a 27-year-old Asian patient, at 8 weeks of gestation, diagnosed with an acute myocarditis. The woman was admitted to the hospital, presenting with early and nonspecific symptoms, (fever up of 38.5 degrees Celsiuss, abdominal pain and nausea). After temporary improvement, the patient's condition deteriorated. On the fourth day of the hospitalization, myocarditis led to heart failure and the patient had to be transffered to the Intensive Care Unit. Wide-spectrum antibiotics, glucocorticoids, diuretics, bisoprolol, as well as fluid and electrolyte supplementation, were administered. After 22 days of treatment the patient was discharged home in good condition. Afterwards she attended follow-up visits at the Gynecology-Obstetric Outpatient Clinic. She delivered a healthy son (2340 grams, 51 centimetres, Apgar 10) at 37 weeks of gestation. At present, she remains under the care of the Cardiac Clinic and requires small doses of bisoprolol because of periodic supraventricular arrhythmias.
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PMID:[Acute heart failure due to myocarditis in the first trimester of pregnancy]. 2403 68


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