Clinical Profile, Acute Care, and Middle-Term Outcomes of Cocaine-Associated ST-Segment Elevation Myocardial Infarction in an Inner-City Community.

Although cocaine is a well-recognized risk factor for coronary disease, detailed information is lacking regarding related behavioral and clinical features of cocaine-associated ST-segment elevation myocardial infarction (STEMI), particularly in socioeconomically disadvantaged urban settings. Nor are systematic or extended follow-up data available on outcomes for cocaine-associated STEMI in the contemporary era of percutaneous coronary intervention. We leveraged a prospective STEMI registry from a large health system serving an inner-city community to characterize the clinical features, acute management, and middle-term outcomes of cocaine-related versus cocaine-unrelated STEMI. Of the 1,003 patients included, 60% were black or Hispanic. Compared with cocaine-unrelated STEMI, cocaine-related STEMI (n = 58) was associated with younger age, male gender, lower socioeconomic score, current smoking, high alcohol consumption, and human immunodeficiency virus seropositivity but less commonly with diabetes or hypertension. Cocaine users less often received drug-eluting stents or ß blockers at discharge. During median follow-up of 2.7 years, rates of death, death or any rehospitalization, and death or cardiovascular rehospitalization did not differ significantly between cocaine users and nonusers but were especially high for death or any hospitalization in the 2 groups (31.4 vs 32.4 per 100 person-years, p = 0.887). Adjusted hazard ratios for outcomes were likewise not significantly different. In conclusion, in this low-income community, cocaine use occurred in a substantial fraction of STEMI cases, who were younger than their nonuser counterparts but had more prevalent high-risk habits and exhibited similarly high rates of adverse outcomes. These data suggest that programs targeting cocaine abuse and related behaviors could contribute importantly to disease prevention in disadvantaged communities.

The proarrhythmic effect of hypoglycemia: evidence for increased risk from ischemia and bradycardia.

Hypoglycemia increases the risk for both overall and sudden death. At a cellular level, hypoglycemia causes alterations in the physiology of myocardial tissue that are identical to proarrhythmic medications. Reduced serum glucose blocks the repolarizing K(+) channel HERG, which leads to action potential and QT prolongation and is uniformly associated with risk for torsades de pointes ventricular tachycardia. The sympathetic response induced by hypoglycemia also increases the risk of arrhythmias from Ca(2+) overload, which occur with sympathomimetic medications and excessive beta adrenergic stimulation. Thus, hypoglycemia can be considered a proarrhythmic event. This review focuses on emerging evidence for two other important changes induced by hypoglycemia that promote arrhythmias: ischemia and bradycardia. Studies of patients with "insulin shock" therapy from the early twentieth century and other more recent data strongly suggest that hypoglycemia can cause ischemia of myocardial tissue, both in association with coronary artery obstructions and by cellular mechanisms. Ischemia induces multiple proarrhythmic responses. Since ischemia itself reduces the possibility of using energy substrates other than glucose, hypoglycemia may generate positive feedback for electrophyisologic destabilization. Recent studies also show that hypoglycemia can cause bradycardia and heart block. Bradycardia is known to cause action potential prolongation and potentiate the development of torsades de pointes, particularly with low-serum K(+) which can be induced by hypoglycemic episodes. Thus, hypoglycemia-induced bradycardia may also create a dynamic, positive feedback for the development of arrhythmias and sudden death. These studies further support the hypothesis that hypoglycemia is a proarrhythmic event.

Prevalence of hemoglobin A1c greater than 6.5% and 7.0% among hospitalized patients without known diagnosis of diabetes at an urban inner city hospital.

CONTEXT: Bronx, New York, an urban county with a large low-income, immigrant and minority population, has a prevalence of diabetes that is among the highest in the United States. OBJECTIVE: The aim of the study was to evaluate the utility of hemoglobin A1c (HbA1c) in identifying patients at risk for diabetes on an in-patient medical service of a hospital serving a high prevalence community. DESIGN AND SETTING: We conducted a prospective cohort study at an urban public hospital. PATIENTS: The study included 971 patients (1132 admissions) admitted to the general medicine service over 4 months. MAIN OUTCOME MEASURES: HbA1c was measured on all patients. Records were checked for prior diagnosis of diabetes and other clinical data. Follow-up data were obtained for those with repeat HbA1c testing or glucose within 1 yr after admission. RESULTS: We found that 35.2% of the patients (n = 342) had an established diagnosis of diabetes. The remaining 629 patients defined the study cohort of patients without known diabetes. Mean HbA1c was 6.05 +/- 0.87%. A total of 152 patients (24%) had admission HbA1c of at least 6.5% and 62 (9.9%) had HbA1c of at least 7.0%. Fifty-five patients with HbA1c of at least 6.5% had follow-up HbA1c within 1 yr. Of those, 44 (80.0%) met the criteria for diabetes as proposed by The International Expert Committee using repeated HbA1c testing. CONCLUSION: In communities with high prevalence of diabetes, a large percentage of patients without a diagnosis of diabetes who are admitted as in-patients have HbA1c of at least 6.5% and 7.0%. Hospital-based HbA1c testing might identify patients for whom further testing is indicated to make the diagnosis of diabetes.

Beta-blockers are associated with reduced risk of myocardial infarction after cocaine use.

STUDY OBJECTIVE: Beta-blocker use is associated with coronary artery spasm after cocaine administration but also decreases mortality in patients with myocardial infarction or systolic dysfunction. We conduct a retrospective cohort study to analyze the safety of beta-blockers in patients with positive urine toxicology results for cocaine. METHODS: The cohort consisted of 363 consecutive telemetry and ICU patients who were admitted to a municipal hospital and had positive urine toxicology results for cocaine during a 5-year period (307 patients). Fifteen patients with uncertain history of beta-blocker use before admission were excluded. The primary outcome measure was myocardial infarction; secondary outcome measure was inhospital mortality. Logistic regression analysis using generalized estimating equations models and propensity scores compared outcomes. RESULTS: Beta-blockers were given in 60 of 348 admissions. The incidence of myocardial infarction after administration of beta-blocker was significantly lower than without treatment (6.1% versus 26.0%; difference in proportion 19.9%; 95% confidence interval [CI] 10.3% to 30.0%). One of 14 deaths occurred in patients who received beta-blockade (incidence 1.7% versus 4.5% without beta-blockade; difference in proportion 2.8%; 95% CI -1.2% to 6.7%). Multivariate analysis showed that use of beta-blockers significantly reduced the risk of myocardial infarction (odds ratio 0.06; 95% CI 0.01 to 0.61). CONCLUSION: In our cohort, administration of beta-blockers was associated with reduction in incidence of myocardial infarction after cocaine use. The benefit of beta-blockers on myocardial function may offset the risk of coronary artery spasm.

Importance of hepatitis C coinfection in the development of QT prolongation in HIV-infected patients.

BACKGROUND: Case reports and unblinded studies suggest that human immunodeficiency virus (HIV) disease is associated with QT prolongation and torsade de pointes ventricular tachycardia. Hepatitis C coinfection is common in patients with HIV disease, and cirrhosis is also associated with QT prolongation. We therefore undertook a systematic analysis of the role of liver injury, nutritional state, and coinfection with hepatitis C in the etiology of QT prolongation in HIV disease. METHODS: We performed a blinded, controlled retrospective cohort study of 1648 patients over a 3-year period at a university-affiliated municipal hospital. All electrocardiograms were included if patients with HIV disease had measurements of CD4 count and viral load within 3 months and serum electrolytes within 30 days (n = 816). Control subjects were chosen randomly from the general medicine service (n = 832). QT interval was measured in lead II and corrected for heart rate by Bazett's formula (QTc). RESULTS: QTc was slightly but significantly longer in patients with HIV disease than in controls (443 +/- 37 vs 436 +/- 36 milliseconds, P < .001). Patients with hepatitis C had more pronounced QTc prolongation (452 +/- 41 vs 437 +/- 35 milliseconds, P < .001). CD4 count, HIV viral load, and HIV medications had no effect on QTc. When patients with hepatitis C were excluded from the analysis, there was no statistical difference between patients with HIV disease and controls (438 +/- 34 vs 436 +/- 36 milliseconds, P = .336). Multiple linear regression revealed that both HIV and hepatitis C infection predicted QTc prolongation, as did age, female sex, history of hypertension, use of opiates, low serum K+ and albumin, and high AST. Hepatitis C coinfection nearly doubled the risk of QTc of 470 milliseconds or greater in patients with HIV disease (29.6% vs 15.8%, P < .001). CONCLUSIONS: Human immunodeficiency virus and hepatitis C infections both independently prolong QTc. Coinfection with hepatitis C greatly increases the likelihood of clinically significant QTc prolongation in patients with HIV disease.

Diabetes and stress hyperglycemia associated with myocardial infarctions at an urban municipal hospital: prevalence and effect on mortality.

Municipal hospitals in large cities provide care for patients from immigrant and mixed ethnic communities that are at high risk for diabetes. Both diabetes and stress hyperglycemia increase the risk of adverse outcome after myocardial infarctions, and the impact of stress hyperglycemia on the outcome of myocardial infarctions in this particular setting has not been previously studied. We therefore undertook a retrospective cohort study to determine the prevalence of diabetes and stress hyperglycemia in patients presenting to a university-affiliated Bronx municipal hospital with myocardial infarction, and the relationship of these conditions to the extent of coronary disease and mortality. We obtained data on 106 consecutive patients from July 1998 to April 1999 with a diagnosis-related group diagnosis of either myocardial infarction or acute coronary syndrome, in which myocardial infarction was confirmed by serum enzymes or characteristic electrocardiographic changes. Patients were followed until March 30, 2001. Measurements of clinical parameters and results of catheterization were obtained for all patients. Death rates were determined by laboratory database, direct patient contact, or data from National Death Index. Eighty percent of the cohort had either a diagnosis of diabetes (n = 45, 42% of cohort) or evidence of stress hyperglycemia (defined as serum glucose greater than 126 mg/dL at the time of admission without prior diagnosis of diabetes, n = 40, 38%). In-hospital mortality for patients with diabetes, stress hyperglycemia, or normal glucose was 20%, 15%, and 14%, respectively. Eighty-three percent of the cohort received beta blockers, and 61% of hospital survivors had catheterization. Left main or triple vessel disease was common in both patients with diabetes (52%) and patients with stress hyperglycemia (32%). Mortality at follow up (maximum follow up 3 years; mean follow up 19.6 months) was much higher in patients with either diabetes (42%) or stress hyperglycemia (52%) than normal subjects (24%). Kaplan-Meier analysis of the difference in mortality between patients with high glucose on admission and normal subjects was borderline significant (P = 0.06). Multivariate regression demonstrated that age (P = 0.020), increase in admission serum creatinine (P = 0.001), and reduction in either ejection fraction (P = 0.016) or admission systolic blood pressure (P = 0.005) were significant predictors of mortality. Glycemic status and sex were not independently associated with death after controlling for these other factors. These results show that the prevalence of both diabetes and stress hyperglycemia on presentation with myocardial infarction is strikingly high in this immigrant, mixed ethnic, urban population. Patients with diabetes and stress hyperglycemia had advanced disease on presentation and much higher mortality at 2 to 3 years than those with normal blood glucose. The mortality difference is the result of older age and more advanced disease rather than hyperglycemia per se.

Community-based screening for cardiovascular disease and diabetes using HbA1c.

BACKGROUND: Persons from inner-city immigrant and mixed-ethnic communities are known to be at high risk for cardiovascular disease and diabetes. Such communities may also be underserved for preventive medical care. The authors hypothesized that hemoglobin A1c (HbA1c) could be used as a screening test for a community-based program to detect new cases of diabetes and persons at risk for diabetes and cardiovascular disease. METHODS: Screenings took place in churches, group homes, shelters, community centers, and street corners of the Bronx. Screening data included history of diabetes, age, ethnicity, body mass index, blood pressure, lipid panel, random glucose, and HbA1c. Data were analyzed for number of cases of new diabetes (HbA1c > or =7%), for patients at risk for diabetes (HbA1c 6%-6.99%), and for associations between HbA1c and other variables. The effect of location of screening and self-reported ethnicity on outcome variables was also analyzed. RESULTS: Seven hundred four persons were screened in 25 different sessions. HbA1c and lipid profile were obtained on 539 persons, which formed the cohort for analysis. Mean HbA1c for the cohort was 6.00%. Thirty-two percent of the cohort had HbA1c of more than 6%, and 11.4% had HbA1c of more than 7%. Excluding known diabetics (13% of cohort), 24% had HbA1c of more than 6%, and 3.4% had HbA1c of more than 7%. HbA1c was significantly correlated with total cholesterol, triglycerides, low-density lipoprotein, systolic blood pressure, body mass index, and age; in all cases, correlation coefficients were higher with HbA1c than with random glucose. In addition, significantly higher cardiovascular disease risk factors were found in persons with HbA1c of more than 6%; 6% may be a threshold value for the metabolic syndrome. Mean HbA1c was higher in persons from the South Bronx (which has a higher poverty rate) than the North Bronx (6.08% v 5.74%, p=0.013). There were no statistically significant differences between self-reported ethnic groupings. CONCLUSIONS: There was a high prevalence of undiagnosed diabetes, and of patients at risk for diabetes, in this community setting. Community-based screening can be used as a method for identifying high percentages of patients at risk for diabetes or with undiagnosed diabetes in an inner city, immigrant, mixed-ethnic population.