QTc prolongation among hospitalized patients receiving methadone.
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Biomedical subjects
Publications and source records attributed to Mori J Krantz.
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BACKGROUND: Secondhand smoke exposure increases the risk of acute myocardial infarction (AMI). One study (Helena, Mont) examined the issue and found a decrease in AMI associated with a smoke-free ordinance. We sought to determine the impact of a smoke-free ordinance on AMI admission rates in another geographically isolated community (Pueblo, Colo). METHODS AND RESULTS: We assessed AMI hospitalizations in Pueblo during a 3-year period, 1.5 years before and 1.5 years after implementation of a smoke-free ordinance. We compared the AMI hospitalization rates among individuals residing within city limits, the area where the ordinance applied, versus those outside city limits. We also compared AMI rates during this time period with another geographically isolated but proximal community, El Paso County, Colo, that did not have an ordinance. A total of 855 patients were hospitalized with a diagnosis of primary AMI in Pueblo between January 1, 2002, and December 31, 2004. A reduction in AMI hospitalizations was observed in the period after the ordinance among Pueblo city limit residents (relative risk [RR]=0.73, 95% confidence interval [CI] 0.63 to 0.85). No significant changes in AMI rates were observed among residents outside city limits (RR=0.85, 95% CI 0.63 to 1.16) or in El Paso County during the same period (RR=0.97, 95% CI 0.89 to 1.06). The reduction in AMI rate within Pueblo differed significantly from changes in the external control group (El Paso County) even after adjustment for seasonal trends (P<0.001). CONCLUSIONS: A public ordinance reducing exposure to secondhand smoke was associated with a decrease in AMI hospitalizations in Pueblo, Colo, which supports previous data from a smaller study.
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BACKGROUND: In contrast to patients who develop acute cardiac tamponade after penetrating trauma, tamponade in medical patients may be accompanied by normal or even elevated systolic blood pressure. This has been attributed to heightened sympathetic nervous system activity. CASE REPORT: We present a case of a medical patient with simultaneous hypertension and cardiac tamponade whose blood pressure fell dramatically after pericardiocentesis. We observed a decrease in normetanephrine levels in our patient concomitant with the decrease in blood pressure. CONCLUSIONS: Our case provides further support for involvement of the sympathetic nervous system in medical patients with hypertensive tamponade. To our knowledge, this is the first case documenting adrenergic status in a patient with a paradoxical decrease in blood pressure after relief of tamponade.
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Peripheral arterial disease (PAD) of the lower extremities is a common and potentially life-threatening manifestation of systemic atherosclerosis. Significant PAD is identified by an ankle brachial index (ABI) < 0.90; its presence is strongly associated with the major modifiable cardiac risk factors. Early detection and treatment of asymptomatic PAD is a current focus of numerous cardiovascular guideline organizations as less than a third of patients report typical claudication symptoms. This has created an ever-increasing treatment gap, whereby millions of eligible patients are inadequately treated. Risk factor management including exercise, smoking cessation, and aggressive treatment of lipids and blood pressure are essential in PAD patients. However, life-long antiplatelet therapy provides additional reductions in vascular events beyond aggressive risk factor management. The use of aspirin as well as more potent antiplatelet therapies such as thienopyridines holds promise for reducing atherothrombosis in this very high-risk population.
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We prospectively assessed the effect of oral methadone on the corrected QT interval (QTc) among 160 patients free of structural heart disease and measured serum methadone concentrations and simultaneous QTc intervals in a subset of 44 participants. Mean +/- SD QTc increased by 12.4 +/- 23 ms (p <0.001) at 6 months, by 10.7 +/- 30 ms (p <0.001) at 12 months, and the QTc change from baseline to 12 months correlated with the trough (r = 0.37, p = 0.008) and peak (r = 0.32, p = 0.03) serum methadone concentrations.
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OBJECTIVE: During the starvation phase of anorexia nervosa (AN), cardiac and skeletal muscle mass decreases, whereas electrocardiographic QT dispersion, a marker of arrhythmia risk, increases. QT dispersion during the chronic phase of AN and its relationship to resting metabolic rate (RMR) have not been described previously and is the subject of the current investigation. METHOD: Six AN patients were compared with 10 age-matched control subjects. Serum electrolyte levels, electrocardiography, anthropomorphic data, and indirect calorimetry were obtained for all participants. RESULTS: Corrected QT interval (QTc) did not differ between groups, but QT dispersion was significantly greater in AN patients. QT dispersion correlated negatively with resting oxygen consumption and RMR. The relationship between QT dispersion and RMR did not persist after correcting for lean body mass. CONCLUSIONS: AN patients with a low RMR may be at risk for increased QT dispersion. QT dispersion is a widely available and inexpensive measure, which may reflect both metabolic status and arrhythmia potential.
OBJECTIVE: Anorexia nervosa (AN) is associated with marked decreases in caloric intake and a corresponding reduction in body weight due to abnormal self body image. Although counterintuitive, hypoalbuminemia and vitamin deficiencies are not expected consequences of this disorder. Etiologic considerations for hypoalbuminemia are discussed. METHOD: The case report of a patient with AN and marked hypoalbuminemia is presented and a focused literature review is reported. RESULTS: Hypoalbuminemia was initially attributed to starvation. However, occult infection was ultimately responsible. Serum albumin concentration normalized with antibiotic therapy despite minimal restoration of body weight. DISCUSSION: Hypoalbuminemia should not be considered a characteristic feature of AN even in the setting of progressive weight loss. The presence of other potentially life-threatening conditions should be sought, as reduced serum albumin concentration is a marker of inflammation in AN.
PURPOSE: Dyslipidemia treatment dramatically decreases coronary heart disease risk in diabetes, yet only a minority of these patients are screened or achieve optimal low-density lipoprotein (LDL) cholesterol levels. Our aim was to increase the percentage of diabetic patients in whom lipid management was achieved through electronic and direct educational detailing. METHODS: The study cohort comprised 884 diabetic patients at 12 primary care practices. Practice sites were randomized to one of three intervention groups: electronic educational detailing, direct (face-to-face) educational detailing, or control. Direct and electronic detailing were performed over a 12-month period. All sites were notified of our goal to enhance lipid testing among diabetic patients. Chart abstraction was performed 15 months after the start of the intervention. For the entire population (n=884), the proportion of patients with lipid testing was calculated, and changes from pre- to postintervention were compared across groups. We compared pre- and postintervention LDL-cholesterol changes between groups using least square means to account for site variation. RESULTS: Favorable provider actions increased significantly with the intervention (+22% compared with +6% in controls, P=.01). By logistic regression, electronic detailing increased the likelihood of lipid testing (odds ratio 3.0, confidence interval 1.6-5.7), as did direct detailing (odds ratio 1.8, confidence interval 0.9-3.7) in patients with no preintervention LDL test (n=432). Lipid testing tended to increase to a greater extent at intervention sites (+23% for the combination of electronic and direct detailing vs +11% for controls, P=.06). CONCLUSIONS: Brief educational detailing either through direct or electronic communication favorably impacts provider behavior regarding dyslipidemia care for diabetic patients.
A patient maintained on methadone for opioid-dependency developed recurrent syncope. Episodes occurred within hours after using cocaine, and were initially presumed secondary to seizure disorder. However, the patient subsequently suffered a cardiac arrest, and polymorphic ventricular tachycardia (torsade de pointes) was documented. Other than cocaine and methadone the patient was receiving no additional agents known to prolong the QT interval. Low serum methadone concentrations and marked reversible left ventricular systolic dysfunction were noted during the hospitalization. These findings, in conjunction with a history of torsade de pointes temporally related to cocaine abuse, suggest that cocaine was a major precipitant of arrhythmia. Recent experimental studies have shown that cocaine and methadone prolong the QT interval through the same mechanism. We examine the effects of cocaine and methadone on cardiac conduction in the context of the opioid-dependent population.
STUDY OBJECTIVE: To evaluate the effects of methadone on QT-interval dispersion. DESIGN: Single-center, prospective, cohort study. SETTING: Methadone maintenance treatment facility. PATIENTS: One hundred eighteen patients who were newly admitted to the facility. Intervention. Twelve-lead electrocardiograms (ECGs) were performed in patients at both baseline and 6 months after the start of methadone therapy. MEASUREMENTS AND MAIN RESULTS: The ECGs were manually interpreted, and investigators were blinded to time interval and methadone dose. At least eight discernible ECG leads were required for study inclusion. Mean differences between baseline and follow-up rate-corrected QT (QTc) interval and QT dispersion were compared. Multivariate associations between clinical characteristics and magnitude of change in QT dispersion were assessed using linear regression. Mean +/- SD baseline QT dispersion was 32.9 +/- 12 msec, which increased to 42.4 +/- 15 msec (+9.5 +/- 18.6 msec, p<0.0001) after 6 months of therapy. The QTc increased by a similar magnitude (+14.1 msec, p<0.0001). No QT dispersion value exceeded 100 msec. The only variable associated with a greater increase in QT dispersion was antidepressant therapy (20 vs 8.5 msec, p=0.04). CONCLUSION: Methadone modestly increased both QTc interval and QT dispersion. Increased QT dispersion reflects heterogeneous cardiac repolarization and occurs with nonantiarrhythmic agents, such as synthetic opioids. However, the magnitude of this effect appears to be substantially less with methadone than with antiarrhythmic drugs.