The Pharmacology and Clinical Use of Lidocaine and Procainamide

Both procainamide and lidocaine are useful for acutely treating cardiac arrhythmias, and procainamide can be useful in chronic antiarrhythmic regimens. Successful management of cardiac arrhythmias requires knowledge of: 1) the mechanism and natural history of the arrhythmia, 2) the physiologic state of the patient, and 3) the cardiac effects, pharmacodynamics, and general pharmacology of the antiarrhythmic drugs

Relationship Between Cardiovascular Disease Knowledge and Race/Ethnicity, Education, and Weight Status

Background: Inadequate cardiovascular disease (CVD) knowledge has been cited to account for the imperfect decline in CVD among women over the last 2 decades. Hypothesis: Due to concerns that at-risk women might not know the leading cause of death or symptoms of a heart attack, our goal was to assess the relationship between CVD knowledge race/ethnicity, education, and body mass index (BMI). Methods: Using a structured questionnaire, CVD knowledge, socio-demographics, risk factors, and BMI were evaluated in 681 women. Results: Participants included Hispanic, 42.1% (n = 287); non-Hispanic white (NHW), 40.2% (n = 274); non-Hispanic black (NHB), 7.3% (n = 50); and Asian/Pacific Islander (A/PI), 8.7% (n = 59). Average BMI was 26.3 ± 6.1 kg/m2. Hypertension was more frequent among overweight (45%) and obese (62%) than normal weight (24%) (P 12 years (both P < 0.0001). Conclusions: Effective prevention strategies for at-risk populations need to escalate CVD knowledge and awareness among the undereducated and minority women

Time course of alpha-1-acid glycoprotein and its relation to myocardial enzymes after acute myocardial infarction

The acute phase reactant, alpha-1-acid glycoprotein, binds to a number of basic antiarrhythmic drugs, including lidocaine, quinidine, propranolol, imipramine and disopyramide. Binding to alpha-1-acid glycoprotein accounts for a decrease in free drug fraction and may alter the expected concentration: response relation of drugs particularly when there are unpredictably large or rapid changes in alpha-1-acid glycoprotein. To determine the time course and magnitude of alpha-1-acid glycoprotein for 1 month after acute myocardial infarction (AMI), blood samples were collected from 27 patients, 14 with AMI and 13 with a chest pain syndrome but no AMI. Patients with AMI had a significant increase in alpha-1-acid glycoprotein after 72 hours (mean 153 ± 35 mg/dl) (p \u3c 0.05), and the maximum was observed on day 7 (mean 165 ± 53 mg/dl) (p \u3c 0.05), returning to baseline by 28 days. There was no significant change in alpha-1-acid glycoprotein in patients with chest pain but no AMI. Regression analysis showed a significant relation between creatine kinase (p \u3c 0.005) and lactic dehydrogenase (p \u3c 0.001) vs alpha-1-acid glycoprotein indicating alpha-1-acid glycoprotein concentration is high in patients with large AMI. Changes in binding resulting from alpha-1-acid glycoprotein during AMI could account for misinterpretation of total drug concentration and response to antiarrhythmic drugs acutely, during convalescence and at discharge. © 1985

Effect of imipramine and nortriptyline on left ventricular function and blood pressure in patients treated for arrhythmias

The effect of imipramine or nortriptyline on left ventricular function and orthostatic blood pressure was evaluated in 20 nondepressed cardiac patients treated for ventricular premature depolarizations (VPDs). Drug was administered by mouth and dose ranging used, 1 mg/kg/day (imipramine) or 0.5 mg/kg/day (nortriptyline), was increased after four doses (imipramine) or six doses (nortriptyline) until \u3e80% suppression of VPDs or adverse effects occurred or until a maximum dose of 5 mg/kg/day (imipramine) or 3.5 mg/kg/day (nortriptyline) was given. Fourteen (70%) had \u3e80% VPD suppression, five had \u3c80% improvement (range 25% to 77%), and one had a VPD frequency increase of 6%. Mean daily imipramine dose was 210 ± 103 mg and mean nortriptyline dose was 100 ± 29 mg. Neither drug significantly changed mean ejection fraction or peak systolic pressure end-systolic volume ratio by radionuclide angiogram. Both reduced standing systolic blood pressure: mean change after imipramine was 26 mm Hg (NS), and after nortriptyline, 14 mm Hg (p \u3c 0.05). Drug was discontinued in two patients because of symptomatic orthostatic blood pressure change \u3e 30 mm Hg. There was not a significant relationship between dose, drug concentration, or functional class and orthostatic change in systolic blood pressure but there was for age (p \u3c 0.05). These observations suggest that even cardiac patients with impaired systolic function may take imipramine or nortriptyline for VPDs; however, frequent blood pressure measurement is advised, particularly in older patients. © 1985