Loss of prazosin effect in severe chronic CHF.
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Biomedical subjects
Publications and source records attributed to J Kjekshus.
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In 60 patients with third degree A-V block, recovery of escape rhythm from overdrive suppression after ventricular pacing has been studied. Implanted unipolar VVI pacemakers were inhibited by chest wall stimuli. A total of 165 rhythmograms were studied. In 37, the rate was irregular, in the other 128 the escape rate increased gradually, following an exponential curve until stabilization after 3 minutes. In 29 of these rhythmograms, a possible exit block of the first escape impulse was observed. In 99 rhythmograms without exit block, escape rhythm recovery time was an average 1.45 times basal escape RR intervals. Overdrive suppression was most marked in patients with a slow escape rhythm.
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Patients being permanently paced for symptomatic AV block were studied by overdrive suppression of the QRS-inhibited pacemaker, in order to observe the underlying heart rhythm. The chest wall stimulation method was used. In complete AV block the escape rhythm recovery time proved highly reproducible on repeated testing on the same day, and in many patients remained so over months or years. Occasionally, a doubling of the escape rhythm recovery time was seen, suggesting initial exit block of the escape focus. Resetting of the escape rhythm usually followed an exponential curve until stabilisation after about 3 minutes. An early escape rhythm with a recovery time of less than 4 seconds was found on every occasion in 21 of 58 patients with complete AV block, and inconstantly in 23 more; in 14 it was never observed. Accidental pacing failure was seen in 15 patients. The overdrive suppression test was helpful in selecting pacemaker dependent patients.
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BACKGROUND: Patients with diabetes mellitus (DM) have a marked increase in coronary heart disease (CHD) events relative to those without DM. In a previous report from the Scandinavian Simvastatin Survival Study using a clinical case definition of DM (n = 202), simvastatin-treated patients had significantly fewer CHD events compared with placebo-treated control subjects. OBJECTIVE: To examine the effect of simvastatin therapy on CHD in patients with DM and impaired fasting glucose levels. METHODS: Using the 1997 American Diabetes Association diagnostic criteria, we assessed the effect of simvastatin therapy post hoc for an average of 5.4 years in Scandinavian Simvastatin Survival Study patients with normal fasting glucose (n = 3237), impaired fasting glucose (n = 678), and DM (n = 483). RESULTS: Simvastatin-treated patients with DM had significantly reduced numbers of major coronary events (relative risk [RR] = 0.58; P = .001) and revascularizations (RR = 0.52; P = .005). Total (RR = 0.79; P = .34) and coronary (RR = 0.72; P = .26) mortality were also reduced in DM, but not significantly, due to small sample size. In impaired fasting glucose (IFG) subjects, simvastatin use significantly reduced the number of major coronary events (RR = 0.62; P = .003), revascularizations (RR = 0.57; P = .009), and total (RR = 0.57; P = .02) and coronary (RR = 0.45; P = .007) mortality. CONCLUSION: Our results extend previous findings in patients with DM to a larger cohort, confirming the benefit of cholesterol lowering with simvastatin treatment on CHD events. In addition, significant decreases in total mortality, major coronary events, and revascularizations were observed in simvastatin-treated patients with impaired fasting glucose levels. These results strongly support the concept that cholesterol lowering with simvastatin therapy improves the prognosis of patients with elevated fasting glucose levels (> or =6.0 mmol/L [> or =110 mg/ dL]) or DM and known CHD.
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In diabetic patients long-term treatment with timolol after myocardial infarction was related to a reduction in overall mortality, total cardiac death, sudden death, and nonfatal reinfarction, compared with patients in a placebo group. The analyses were based on 99 diabetic patients in the Norwegian timolol multicenter study. The dosage of timolol was 10 mg twice daily and the follow-up period was 12-33 mo (mean: 17 mo). When analyzing all randomized patients, there were 14 deaths in the placebo group and 6 deaths in the timolol group, a reduction of 62.8% (P less than 0.05). The number of nonfatal reinfarctions was 10 in the placebo group and 2 in the timolol group, a reduction of 82.7% (P less than 0.05). With regard to inclusion rate, side effects, withdrawals, and timolol-related reduction in mortality and reinfarction, the diabetic patients basically behaved like nondiabetic patients. The data were analyzed retrospectively and should be confirmed by a prospective study. The study also indicates that long-term treatment with timolol may induce slight carbohydrate intolerance.