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)

We report the case of an invasive thymoma presenting as an aortic dissection in a 49-year-old woman with hypertension and a marfanoid appearance. The patient presented to the emergency department with "tearing" substernal chest pain. A chest radiograph revealed a right para-aortic bulge consistent with a dissecting aorta, but an aortogram was normal. Other disease states, including various types of mediastinal masses, have been reported to mimic aortic dissection.
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PMID:Invasive thymoma presenting as aortic dissection. 195 11

1. A novel formulation of nicardipine (25% standard, 75% sustained release--SR) was evaluated in mild hypertension in a double-blind, randomized, placebo-controlled comparison with standard nicardipine (STD), using clinic measurements (Hawksley) augmented by home recorded blood pressures (Copal UA 251). 2. At 2 h after dosing (peak effect) both STD nicardipine (30 mg three times daily) and SR nicardipine (60 mg twice daily) for 28 days produced a highly significant reduction in sitting and standing blood pressure. The mean sitting blood pressure was reduced by 20/16 mm Hg (STD) and by 25/18 mm Hg (SR) compared with placebo. 3. Predose (8-11 h after last dose of STD, 12-15 h after last dose of SR) the reductions in sitting blood pressure relative to placebo were 11/6 mm Hg (STD) and 14/7 mm Hg (SR). 4. Home recordings confirmed the hypotensive effect of both formulations. Both exhibited a distinct 'peak dose' effect between 1-3 h after dosing. The effect of the SR formulation was sustained throughout the 12 h dosing interval. 5. Of the 60 patients entering the study, one died of unexplained staphylococcal septicaema, two were withdrawn for non drug-related reasons and 14 (32%) were withdrawn because of adverse effects on active therapy (headaches, facial flushing, leg oedema, chest pain, dizziness). 6. In the 43 patients who completed the study adverse symptoms were reported more frequently while they were on the two active formulations of nicardipine compared with placebo. Most of these reactions were again of vasodilator origin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nicardipine sustained release in hypertension. 195 36

A 59 year-old housewife was admitted to the emergency service with a sudden onset of chest pain and nausea. Initially she was treated as an acute myocardial infarction, but conventional treatments were not effective, and she was sent to our hospital for further evaluation. Her ECG showed several abnormal findings including T-wave inversion, atrial flutter, QT-time prolongation, ST-segment depression or elevation, and frequent ventricular ectopic beats. The echocardiogram, 201thallium scintigram and coronary angiography were almost normal. Both urinary and plasma levels of catecholamines were remarkably increased, and the plasma epinephrine was extremely high during attacks. Abdominal echotomography and CT-scanning showed a large left adrenal tumor. The 131MIBG scintiscan revealed a high accumulation in this tumor. Then the patient was diagnosed as having pheochromocytoma and catecholamine-induced myocarditis. The administration of phentolamine (10 mg) normalized the inversion of T-wave and the high blood pressure. But when propranolol (2 mg) was administrated in addition to phentolamine, the ECG showed a biphasic low T-wave change. According to these phenomena, we supposed that the alpha-adrenergic receptor was involved in the development of the ST-T changes of the ECG, and the alpha-adrenergic receptor of this patient might be sensitive under excessive catecholamines, according to the inhibition of the beta-receptor by propranolol.
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PMID:[A case of pheochromocytoma with an AMI-like ECG change corrected by an alpha-blocking agent]. 196 1

In this study, we tried to characterize the changes in left ventricular (LV) function and coronary hemodynamics in patients with compensated hypertension (HT) who were free from coronary artery disease. The study group consisted of 10 men with compensated essential HT at ages 48-65 years (mean = 58). The durations of HT history for the various patients ranged from 5 to 14 years. Mean arterial pressure (MAP) was 122 +/- 2 mmHg at the time of study. The control group was composed of 8 men with mild mitral valve prolapse. They were studied because of chest pain with no demonstratable pathological conditions. Their ages ranged from 39 to 65 years (mean = 57). The MAP for controls was 86 +/- 3 mmHg. All patients in both groups underwent routine cardiac catheterization, coronary arteriography, and measurements of the coronary sinus (CS) and great cardiac vein (GCV) blood flows. Left ventricular muscle mass (LVMM), coronary resistance and coronary reserve were also derived from the hemodynamic study. There was a significant difference in the LVMM index between the study patients (114.9 g/m2) and the control subjects (96.8 g/m2, p less than 0.001). The LV function of the patients in the study group was essentially normal, but the following parameters were significantly different from those of the control subjects: cardiac index, stroke volume index, and dp/dtmax. There was a good correlation between repeated measurements of both the CS and GCV blood flows (r = 0.97 for both).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The coronary hemodynamics and left ventricular function in patients with compensated hypertension. 197 57

Since 1988, 641 black and 11,892 white patients with chest pain of presumed cardiac origin have been admitted to coronary care units in 19 hospitals in metropolitan Seattle. Black men and women were younger (58 vs 66, p less than 0.0001), more often admitted to central city hospitals (p less than 0.0001), and developed evidence of acute myocardial infarction (AMI) less often (19 vs 23%, p = 0.01). In the subset of 2,870 AMI patients, blacks (n = 121) were younger (59 vs 67, p less than 0.0001) and had less prior coronary artery bypass graft surgery (2 vs 10%, p = 0.005) and more prior hypertension (67 vs 46%, p less than 0.0001). During hospitalization, whites (n = 2,749) had higher rates of coronary angioplasty (18 vs 10%, p = 0.03) and coronary artery bypass graft surgery (10 vs 4%, p = 0.04), although thrombolytic therapy and cardiac catheterization were used equally in the 2 groups. Hospital mortality was 7.4% for black and 13.1% for white patients (p = 0.07). However, after adjustment for key demographic and clinical variables by logistic regression, this difference was not as apparent (p = 0.38). Questions about the premature onset of coronary artery disease, excess systemic hypertension, and the differential use of interventions in black persons have been raised by other investigators. Despite differences in age, referral patterns and the use of coronary angioplasty and bypass surgery, black and white patients with AMI in metropolitan Seattle had similar outcomes.
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PMID:Characteristics of black patients admitted to coronary care units in metropolitan Seattle: results from the Myocardial Infarction Triage and Intervention Registry (MITI). 198 98

To determine the clinical, laboratory and hemodynamic profile in patients with primary pulmonary hypertension and associated portal hypertension, 7 new cases and 71 previously reported cases were analyzed. There was no gender predilection and the average age at diagnosis was 41 years. Liver cirrhosis was the most frequent cause of hypertension (82%) and a surgical portosystemic shunt was present in 29%. Almost invariably, portal hypertension either preceded or was diagnosed concurrently with pulmonary hypertension, favoring the hypothesis that in portal hypertension, the pulmonary vasculature may be exposed to vasoactive substances normally metabolized or produced by the diseased liver, possibly inducing vasoconstriction or direct toxic damage to the pulmonary arteries. Clinically, exertional dyspnea was the most frequent presenting symptom (81%); other symptoms, such as syncope, chest pain and fatigue, were present in less than 33%. An accentuated pulmonary component of the second heart sound (82%) and a systolic murmur (69%) were the most common physical findings. At least 75% of these patients had evidence of pulmonary hypertension on electrocardiography (right ventricular hypertrophy) or roentgenography (cardiomegaly or dilated main pulmonary arteries, or both). Hemodynamic findings included severe pulmonary hypertension (mean pulmonary artery pressure 59 +/- 19 mm Hg) with normal pulmonary capillary wedge pressure and cardiac output. Treatment was basically palliative and the mean and median survival times were 15 and 6 months, respectively. In brief, on the basis of clinical presentation and laboratory features, patients with combined primary pulmonary hypertension and portal hypertension seldom represent a diagnostic challenge. Further research is needed on treatment, which remains palliative. The survival rate is poor and worse than that seen in isolated primary pulmonary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association between primary pulmonary hypertension and portal hypertension: analysis of its pathophysiology and clinical, laboratory and hemodynamic manifestations. 199 8

A forty-two-year-old man was admitted because of chest pain. Electrocardiograms at admission showed horizontal ST depression in leads, II, III, aVF, V4, V5, and V6. Direct blood pressure monitoring revealed cyclic change between 160/100 mmHg and 70/50 mmHg and heart rate between 80/sec and 120/sec at fifteen minute intervals. The plasma norepinephrine and epinephrine concentrations were elevated during the episodes of hypertension. Pheochromocytoma was found in the right adrenal gland. These cyclic changes in blood pressure and heart rate are an aid for diagnosis.
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PMID:Pheochromocytoma with electrocardiographic change mimicking angina pectoris, and cyclic change in direct arterial pressure--a case report. 200 62

In 88 of 103 consecutive patients with angina and normal coronary arteries, follow-up data could be achieved 6-11 years (9.2 +/- 1.2 years) after diagnostic left heart catheterization. Three of these patients died during follow-up (two noncardiac deaths and one death with no identifiable etiology). One patient suffered a documented myocardial infarction. In 40 patients (47%) chest pain diminished, while symptoms were unchanged in 20 (24%) or even worse in 25 (29%). Resolution or persistence of chest pain could not be predicted either by the character of pain (typical vs. atypical), the presence of hypertension, a left bundle-branch block, a positive exercise electrocardiogram or pathological pulmonary artery pressures during exercise, documentation of myocardial bridges, local wall motion abnormalities, or a left ventricular end-diastolic pressure greater than or equal to 13 mmHg. However, continuing chest pain was significantly more common in patients who revealed a 'slow-flow phenomenon' at initial coronary arteriogram. Thus, in patients with angina and normal coronary arteries the long-term course regarding frequency of morbid cardiac events is benign. However, more than half of the patients reported chest pain to be similar or even worse than at catheterization. Most clinical and invasive results at initial evaluation had no predictive value for the persistence of symptoms. The impact of 'slow-flow' in coronary arteriography, which was a phenomenon almost exclusive to patients with constant or even worse chest pain at follow-up, should be evaluated in larger patient populations.
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PMID:Long-term clinical course of patients with angina and angiographically normal coronary arteries. 203 6

Important features of the racial patterns in CHD at the present time are summarized in Table 15-10. Many of these conclusions follow inevitably from the economic disadvantage suffered by blacks, and the overwhelming importance of hypertension in this population. More knowledge is needed regarding the value of standard diagnostic tools in distinguishing noncoronary from coronary chest pain symptoms. A hard look is also needed at questions of access for blacks, particularly to angioplasty and thrombolytic therapy. There is additional growing evidence that the gains against CHD have been concentrated primarily among the educated and affluent. New strategies will need to be developed if we are to repeat the kind of gains against cardiovascular disease among blacks in the 1990s that were made in the 1970s and 1980s.
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PMID:Coronary heart disease: black-white differences. 204 5

A clinicopathological analysis of myocardial infarction with an onset of stroke-like symptoms was carried out on 30 autopsy cases at the Tokyo Metropolitan Geriatric Hospital. The cases were classified into four groups according to the types of brain lesions, I: embolism (n = 17), II: thrombosis (n = 9), III: bleeding (n = 2), and IV: no remarkable focal lesion (n = 2). Classification was made based on clinical findings, and pathological features. The characteristic clinical findings were conciousness disturbance, no elevation of blood pressure at the onset of stroke, hemiplegia and shock. However, the typical anginal chest pain was found in only 17% of cases. The underlying diseases and complications were hypertension, atrial fibrillation (Af), disseminated intravascular coagulation (DIC), renal failure, malignant neoplasma, and diabetes mellitus. The incidences of Af, DIC, mural thrombus, non-bacterial thrombotic endocarditis (NBTE) were significantly higher in the group with cerebral embolism than in the group with cerebral thrombosis. The coronary stenotic index was also smaller in the group with cerebral embolism. Therefore, the major etiology of cardio-cerebral apoplexy was a simultaneous embolism to the brain and heart due to Af, NBTE or, DIC.
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PMID:[Myocardial infarction beginning with cerebral symptoms in 30 cases of cardio-cerebral apoplexy]. 204 62


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