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

A syncope was the first symptom of aortic rupture in a patient with chronic arterial hypertension. This syncope was the consequence of an acute haemopericardium which resulted in a sudden drop of the cardiac output. Urgent echocardiographic examination in the emergency room made early diagnosis and life-saving pericardiocentesis possible.
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PMID:Successful treatment of aortic rupture presenting as a syncope: the role of echocardiography in diagnosis. 362 28

Of 1,643 cranial computed tomography (CT) scans done in a primary-tertiary care private hospital over a 1-year period, 11 (0.67%) showed diffuse confluent white matter lucencies of less than 30 Hounsfield units. By retrospective analysis, at least 4 of the 11 were demented. Of these, 3 had clinical evidence of Binswanger's disease--characterized by progressive dementia, incontinence, variable pseudobulbar signs, and acute and subacute motor deficits. Two additional patients suffered only transient ischemic attacks or lacunar strokes; 2 had syncope; 1 had multiple sclerosis. The remaining patients were neurologically asymptomatic. In this small retrospective series, the severity of CT changes did not distinguish the patients with clinical Binswanger's syndrome from neurologically less symptomatic patients. Ten of the eleven patients had disordered blood pressure regulation--hypertension, labile systolic pressure, orthostatic hypotension, or a combination of these factors. The severity of CT changes correlated more clearly with blood pressure instability than with clinical encephalopathy. Asymptomatic adult patients with unexplained CT white matter hypodensity and blood pressure disorders may, however, be at risk for the development of subsequent subacute arteriosclerotic encephalopathy.
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PMID:White matter lucencies on computed tomography, subacute arteriosclerotic encephalopathy (Binswanger's disease), and blood pressure. 362 49

Evidence is reviewed linking clinical effects of ethanol with actions on the sympathetic and parasympathetic nervous systems. The studies reported include a series of investigations by the authors. Acutely, ethanol causes peripheral vasodilation and may also result in changes in heart rate and blood pressure. Ethanol may contribute to acute problems which may present clinically, including micturition syncope, accidental hypothermia and facial flushing. However, increased sympathetic nervous activity plays a role in causing hypertension and other symptoms during ethanol withdrawal in chronic alcoholics. Some chronic alcoholics may have neuropathy involving sympathetic nerves, and this can result in distal sweating loss and occasionally in orthostatic hypotension. Also, hypothalamic lesions associated with Wernicke's encephalopathy may result in hypothermia. Neuropathy involving parasympathetic nerves in not uncommon in alcoholics with other evidence of nervous system damage, but it is generally asymptomatic. Occasionally, vagal neuropathy may cause disorder of gastrointestinal motility, and neuropathy affecting the sacral innervation may be a factor in alcoholic impotence.
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PMID:The effects of acute and chronic ingestion of ethanol on the autonomic nervous system. 381 27

The incidence, risk factors and long-term prognosis of complex ventricular arrhythmias after coronary artery bypass graft surgery are not known. Complex ventricular arrhythmias are defined as Lown grades 4a (couplets), 4b (ventricular tachycardia) and 5 (R on T phenomenon). Ninety-two patients with normal left ventricular function who underwent elective coronary artery bypass graft surgery were prospectively evaluated. Ventricular arrhythmias were documented by predischarge 24 hour ambulatory electrocardiographic monitoring; 43% of patients had no or simple ventricular arrhythmias (Lown grades 1 to 3) and 57% had complex ventricular arrhythmias. Risk factors analyzed included age, sex, diabetes, hypertension, smoking, preoperative digoxin or propranolol therapy, cardiopulmonary bypass time, aortic cross-clamp time, number of vessels bypassed, peak creatine kinase (CK) elevation and pericarditis. No risk factor identified patients at higher risk for complex ventricular arrhythmias. Patients were followed up for 6 to 24 months (mean 16). Patients with complex ventricular arrhythmias did not have a higher incidence of sudden death, cardiac death, syncope, angina, myocardial infarction or cerebrovascular accident. It was concluded that: Complex ventricular arrhythmias are common after coronary artery bypass graft surgery. None of the risk factors considered identify high risk patients. Complex ventricular arrhythmias after coronary artery bypass graft surgery do not indicate a poor prognosis in patients with normal left ventricular function.
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PMID:Ventricular arrhythmias after coronary artery bypass graft surgery: incidence, risk factors and long-term prognosis. 387 91

Among 509 patients referred to our Institute for Holter monitoring, between 1st September, 1982-30th October, 1983, 28 patients aged 65-90 (mean 76) were referred for dizziness and syncope. There were 17 men and 11 women. Seven patients had a M.I. in their past, 4 angina pectoris, 5 hypertension, 4 aortic stenosis or aortic insufficiency or both, hemodynamically significant, one had mitral valve prolapse (MVP) and one transient ischemic attacks (TIA). In our series 16 out of 28 patients received digoxin and antiarrhythmic drugs (quinidine, propranolol, procainamide, Neo-gilurythmal, amiodarone), 2 of them digoxin and quinidine in full doses and one digoxin and amiodarone. Other drugs administered to our patients included Aldomin, Isordil, Lasix, aminophylin, cromoglycate etc. In 10 patients (35.7%) we found complex ventricular arrhythmias (7 with M.I., 3 patients of 4 with significant aortic valve lesion, 2 patients of 2 with left anterior hemiblock (LAH), 1 patient with MVP, 1 patient with TIA). In another 5 patients (17.8%) we found atrial fibrillation, fast rhythm (2 with chronic obstructive lung disease, 2 with hypertension and 1 in post M.I.) which explained their symptomatology. From our data we conclude that the pluripathology found in old age as well as the multimedication administered, cause a plurietiology of syncope, arrhythmias playing an important role in its determination, in this particular age group.
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PMID:Holter monitoring for dizziness and syncope in old age. 387 98

A retrospective study was conducted of 101 hospitalized patients who had one or more episodes of syncope. The etiology of syncope was established with relative ease in 61% of these patients. History and physical examination revealed the cause in 34%, resting ECG in 11% and 24-h ECG monitoring in 16%. Additional tests (electroencephalograms, Doppler studies of the cervical arteries, computerized tomography of the brain, ultrasonography of the heart and cardiac catheterization) either were noncontributory or did not contribute to confirmed diagnoses already established by other means. Cardiac causes were responsible for the syncope in 34% and noncardiac causes in 27%. Comparison between diagnosed and undiagnosed patients revealed no significant differences with respect to age, number of syncopal episodes or presence of hypertension or diabetes. There were, however, significantly more women, and a lower frequency of ischemic heart disease and other associated diseases in the undiagnosed group. It is concluded that all patients with syncope should undergo ambulatory ECG and 24-h ECG monitoring, and that hospitalization should be reserved for patients whose clinical condition requires admission or when further investigation is necessary.
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PMID:Syncope: a retrospective study of 101 hospitalized patients. 391 52

The clinical and electrophysiological features and the natural history of median intra-His block with a normal resting electrocardiogram were studied: 11 patients had a fixed split H1-H2 potential with a spontaneous or induced block between H1 and H2. The patients (5 men and 6 women) were aged 17 to 70 years (average 53 years). Associated pathology included 2 cases of aortic stenosis (1 severe), 1 case of ischaemic heart disease (effort angina), 1 case of mitral valve prolapse and 2 cases of hypertension. The presenting symptoms were syncope (4 cases), dizziness (2 cases), effort angina (1 case) and tiredness (3 cases); 1 patient was asymptomatic. Holter monitoring (24 hours) was performed in 8 patients and s-owed paroxysmal conduction defects in 6 cases; 4 Mobitz II 2nd degree AV block, 1 3rd degree AV block with narrow QRS complexes and 1 case of blocked atrial extrasystoles at coupling intervals longer than 480 ms and sinus cycle lengths of over 800 ms. Exercise testing by bicycle ergometry (4 patients) was normal in 1 case and revealed Mobitz II 2nd degree AV block in 3 cases. Baseline electrophysiological studies showed an A-H1 interval ranging from 60 to 100 ms (average 78 ms), a H1-H2 interval of 20 to 40 ms (average 31 ms) and a H2-V interval of 30 to 50 ms (average 32 ms). Block between H1 and H2 was observed: "spontaneously" during electrophysiological investigation in 6 cases, after IV atropine in 1 case, during overdrive atrial pacing at rates slower than 150/min in 7 cases, after atrial extrastimulus with a functional intra-His refractory period of over 420 ms in 7 cases, after ajmaline in 3 of the 4 cases in which this test was performed. A cardiac pacemaker was implanted in 10 patients in whom the initial symptoms have all regressed; the remaining patient considered to be "epileptic" had another syncopal attack under therapy and was finally paced. This series demonstrates that the diagnosis of median intra-His block depends on precise electrophysiological criteria and should be looked for even when the presenting symptoms are atypical; some of our patients complained only of tiredness. The value of Holter monitoring and careful endocavitary investigation is emphasised. Median intra-His block should be distinguished from longitudinal and functional His bundle dissociation.
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PMID:[Clinical and electrophysiological aspects of median intra-His bundle block with normal electrocardiogram at rest]. 392 29

Closed-chest trauma in a young man was followed by rupture of a right ventricular papillary muscle and bifascicular block. This produced signs and symptoms of tricuspid regurgitation and recurrent syncope. Treatment by valve replacement and pacemaker implantation was successful. Review of 30 cases of traumatic tricuspid regurgitation reveals that this patient had characteristic findings: adult onset of isolated tricuspid regurgitation, a history of trauma, right bundle branch block, and cardiomegaly without signs of left ventricular failure. In addition, right atrial hypertension of longstanding may produce cyanosis because of right-left shunting through a patent foramen ovale.
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PMID:Chronic tricuspid regurgitation and bifascicular block due to blunt chest trauma. 394 68

We studied 36 patients (21 women and 15 men) with spontaneous dissection of the internal carotid arteries. The ages of these patients ranged from 21 to 63 years. Focal unilateral headache was the most common symptom. Other common clinical manifestations (in decreasing order of frequency) included focal cerebral ischemic symptoms, oculosympathetic paresis, bruits, light-headedness, and neck pain. Less common symptoms were syncope, amaurosis fugax, scalp tenderness, swelling in the neck, and dysgeusia. Common angiographic manifestations (in decreasing order of frequency) were elongated, irregular, and frequently tapered narrowing of the lumen; abrupt luminal reconstitution (often at the carotid canal); aneurysms; intimal flaps; slow internal carotid artery--middle cerebral artery flow; tapered occlusion; and distal branch occlusions. The incidence of hypertension in these patients was considerably higher than that in the general population. Angiographic evidence of fibromuscular dysplasia was found in 14% of the patients, but atherosclerotic changes were uncommon. Follow-up ranged from 14 to 140 months (mean, 58.5 months). Twenty-three patients with 29 dissected internal carotid arteries were also restudied angiographically. The stenosis of the internal carotid artery either completely resolved or substantially improved in more than 85% of the dissected vessels. About two-thirds of the dissecting aneurysms either resolved or decreased in size. Clinically more than 85% of the patients had an excellent or complete recovery. Recurrence of the dissection or rupture of a dissecting aneurysm was not noted. Despite their disconcerting appearance on angiography, spontaneous dissections of the internal carotid arteries are often associated with a good prognosis.
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PMID:Spontaneous dissection of the cervical internal carotid artery. 396 55

We present a case of a 79-year-old woman with periods of syncope, complete heart block (CHB), and ventricular standstill during periods of increased vagal tone following sublingual nifedipine for hypertension. The syncopal episodes were associated with periods of elevated vagal tone (micturition and vomiting) with one monitored episode showing a clear time course of emesis; CHB then ensued, progressing to ventricular standstill with loss of consciousness that resolved over several minutes. Although nifedipine is not thought to affect conduction at current clinical dosages, it seems likely that the additive effects of nifedipine and elevated vagal tone produced the observed conduction abnormalities. This is the first case report of nifedipine administration followed by syncope and conduction disturbances.
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PMID:Syncope and conduction disturbances following sublingual nifedipine for hypertension. 403 65


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