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PubMed · 10434616

[Essential tremor].

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T Hashimoto. 1999. [Essential tremor].. https://pubmed.ncbi.nlm.nih.gov/10434616/

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Gender differences in the management and outcome of acute myocardial infarction in unselected patients in the thrombolytic era.

This study compares the clinical features, management, and outcome in men and women from a consecutive, unselected series of patients with acute myocardial infarction (AMI) who were admitted to a university cardiac center over a 3-year period. It is a retrospective observational study of 1,059 admissions with AMI identified through the Hospital In-Patient Enquiry (HIPE) registry, validated according to Minnesota Manual criteria, and followed for a period of up to 5 years (median 36 months). Women comprised 40% of all admissions, had a higher hospital mortality (24% vs. 16%, p<0.001), and were less likely to receive thrombolysis (23% vs. 33%, p<0.01), admission to coronary care (65% vs. 77%, p<0.001), or subsequent invasive or noninvasive investigations (55% vs. 63%, p<0.01). However, women with AMI were older than men with AMI (71 vs. 65 years, p<0.001). After adjusting for age, differences that remained significant were prevalence of hypertension (odds ratio [OR] 2.12, 95% confidence intervals [CI] 1.56 to 2.88) and cigarette smoking (OR 0.47, 95% CI 0.35 to 0.65), management in coronary care (OR 0.66, 95% CI 0.49 to 0.88), and hospital mortality (OR 1.48, 95% CI 1.07 to 2.04). Excess mortality occurred predominantly in women <65 years old (18% vs. 8%, OR [multivariate] 2.35, 95% CI 1.19 to 4.56), among whom multivariate analysis demonstrated a significantly lower thrombolysis rate (OR 0.48, 95% CI 0.27 to 0.86). In this group, lack of thrombolysis independently predicted hospital mortality (OR 5.37, 95% CI 1.45 to 19.82). Female gender was not an independent predictor of mortality following AMI (OR 1.42, 95% CI 0.90 to 2.26). Thus, among unselected patients, female gender is associated with, but not an independent predictor of, reduced survival after AMI. Gender differences in mortality are greatest in younger patients, who are less likely to receive thrombolysis and in whom lack of thrombolysis is independently associated with mortality after AMI.

Adrenergic beta-Antagonists

Nerve sprouting and sudden cardiac death.

The factors that contribute to the occurrence of sudden cardiac death (SCD) in patients with chronic myocardial infarction (MI) are not entirely clear. The present study tests the hypothesis that augmented sympathetic nerve regeneration (nerve sprouting) increases the probability of ventricular tachycardia (VT), ventricular fibrillation (VF), and SCD in chronic MI. In dogs with MI and complete atrioventricular (AV) block, we induced cardiac sympathetic nerve sprouting by infusing nerve growth factor (NGF) to the left stellate ganglion (experimental group, n=9). Another 6 dogs with MI and complete AV block but without NGF infusion served as controls (n=6). Immunocytochemical staining revealed a greater magnitude of sympathetic nerve sprouting in the experimental group than in the control group. After MI, all dogs showed spontaneous VT that persisted for 5.8+/-2.0 days (phase 1 VT). Spontaneous VT reappeared 13.1+/-6.0 days after surgery (phase 2 VT). The frequency of phase 2 VT was 10-fold higher in the experimental group (2.0+/-2.0/d) than in the control group (0.2+/-0.2/d, P<0.05). Four dogs in the experimental group but none in the control group died suddenly of spontaneous VF. We conclude that MI results in sympathetic nerve sprouting. NGF infusion to the left stellate ganglion in dogs with chronic MI and AV block augments sympathetic nerve sprouting and creates a high-yield model of spontaneous VT, VF, and SCD. The magnitude of sympathetic nerve sprouting may be an important determinant of SCD in chronic MI.

Adrenergic beta-Antagonists

Are beta-blockers effective in elderly patients who undergo coronary revascularization after acute myocardial infarction?

BACKGROUND: Although randomized clinical trials have demonstrated that beta-blocker therapy is effective in reducing mortality after acute myocardial infarction (AMI), many of these studies excluded patients who undergo coronary revascularization. However, the clinical practice guidelines established by the American College of Cardiology and the American Heart Association recommend that beta-blocker therapy be considered for patients who underwent successful revascularization after AMI. METHODS: Using data from the Cooperative Cardiovascular Project, we compared the initiation of beta-blocker therapy at discharge in patients aged 65 years or older who underwent coronary artery bypass surgery (CABG) or percutaneous transluminal coronary angioplasty (PTCA) during their hospitalization for AMI with that of patients who did not undergo revascularization. We then examined whether beta-blocker therapy was associated with lower 1-year mortality between revascularized and nonrevascularized groups. RESULTS: After excluding patients with contraindications to beta-blocker therapy, 84 457 patients remained in the study sample. Of these, 8482 patients underwent CABG, and 13 997 patients underwent PTCA. After adjusting for demographic and clinical factors, we found that these patients were less likely to initiate beta-blocker therapy after CABG (odds ratio [OR], 0.44; 95% confidence interval [CI], 0.41-0.47) or PTCA (OR, 0.89; 95% CI, 0.85-0.93) relative to the nonrevascularized group. After adjusting for potential confounders, beta-blockers were significantly associated with lower 1-year mortality in patients who underwent CABG (hazard ratio [HR], 0.70; 95% CI, 0.55-0.89) or PTCA (HR, 0.86; 95% CI, 0.74-1.00), similar to that of the non-revascularized group (HR, 0.83; 95% CI, 0.80-0.87). CONCLUSIONS: Therapy after AMI with beta-blockers appears to be as effective in reducing 1-year mortality for elderly patients who have undergone CABG or PTCA as for a nonrevascularized group. Our findings suggest that routine use of beta-blockers should be considered for patients who undergo revascularization after AMI.

Adrenergic beta-Antagonists