Andres R. Palomo

Cardiovascular findings in quadriplegic and paraplegic patients and in normal subjects

Abstract Seven normal, 7 paraplegic and 7 quadriplegic patients underwent cross-sectional cardiovascular evaluation, including recording of sitting heart rate, blood pressure and echocardiography. Quadriplegic patients had a 26% lower left ventricular (LV) mass index (75 ± 13 g/m 2 , p 2 ) or paraplegic patients (110 ± 26 g/m 2 ). Six quadriplegic patients and 3 paraplegic patients had an unusual pattern of LV posterior wall asynergy, which was associated with a significant rightward shift of the frontal-plane QRS axis (92 ± 22 ° vs 42 ± 41 °, p

Increased quinidine plasma concentrations during administration of verapamil: A new quinidine-verapamil interaction

Abstract A number of drug interactions that involve quinidine have been reported. 1 These include both pharmacokinetic interactions in which plasma concentrations of other drugs, most notably digoxin, are influenced by quinidine, and pharmacologic interactions. The latter is exemplified by a recent report of marked hypotension when intravenous verapamil was given to patients receiving oral quinidine preparations. 2 This hypotension was presumably due to α-adrenergic blockade and the peripheral vasodilatation was a result of both quinidine and verapamil. We report a patient with cyanotic congenital heart disease and atrial flutter with 1:1 atrioventricular conduction who had a previously unreported quinidine-verapamil pharmacokinetic interaction.

Procainamide pharmacokinetics in patients with acute myocardial infarction or congestive heart failure

Abnormal procainamide pharmacokinetics (prolonged half-life and decreased volume of distribution) and pharmacodynamics (decreased threshold for the suppression of premature ventricular complexes) have been suggested in patients with acute myocardial infarction or congestive heart failure, or both. To better define procainamide kinetics, 37 patients in the acute care setting received intravenous procainamide (25 mg/min, median dose 750 mg) with peak and hourly blood samples taken over 6 hours. Compared with the 10 control patients, the 12 patients with acute myocardial infarction and the 15 patients with congestive heart failure had normal procainamide pharmacokinetics with respect to half-life (2.3 +/- 1.0, 2.5 +/- 0.9 and 2.6 +/- 0.8 hours, respectively), volume of distribution (1.9 +/- 0.7, 1.8 +/- 0.4 and 1.8 +/- 0.5 liters/kg, respectively), clearance (11.3 +/- 7.5, 9.3 +/- 3.6 and 9.1 +/- 3.5 ml/min per kg, respectively) and unbound drug fraction (66 +/- 9, 66 +/- 9 and 69 +/- 4%, respectively). Low thresholds for greater than 85% premature ventricular complex suppression were confirmed in these patients (median 4.7 micrograms/ml in patients with acute myocardial infarction and 3.3 micrograms/ml in patients with congestive heart failure). Thus, differences in the response of premature ventricular complexes to procainamide reflect electropharmacologic differences dependent on clinical setting rather than pharmacokinetic abnormalities. Furthermore, the reduction of procainamide dosing in patients with acute myocardial infarction or congestive heart failure, based solely on prior kinetic data, may result in inappropriate antiarrhythmic therapy.

Cardiac arrhythmias associated with prophylactic pacing during coronary angiography

Data from 518 consecutive cardiac catheterizations were analyzed to test the value of prophylactic pacemaker insertion during coronary angiography and to compare the incidence of arrhythmic complications in patients with and without pacemakers. In patients without pacing (n = 273), 1 episode of ventricular fibrillation occurred, which responded promptly to defibrillation. Sinus bradycardia (fewer than 30 beats/min for 10 seconds) was recorded in 74 patients (27%) and required treatment in 30 (11%). No patient required or would have benefited from pacemaker placement. Of the 245 patients with prophylactic pacemakers, there was an increased incidence of all ventricular (9 vs 1; p less than 0.013) and supraventricular (5 vs 0; p less than 0.046) arrhythmias. Pacemaker-associated induction of ventricular fibrillation occurred in 2 patients and was clearly related to electrical stimulation during a normally non-vulnerable period of the cardiac cycle. In conclusion, routine prophylactic pacemaker insertion during coronary angiography is not warranted in patients with normal sinus rhythm and normal atrioventricular conduction. More information is needed to determine if pacing is needed in patients with conduction system disease.

Correlates of Atherosclerosis in Coronary Arteries of Patients Undergoing Angiographic Evaluation

The correlations between lipid and lipoprotein measurements and other risk factors of coronary artery disease were evaluated in 101 men undergoing coro nary angiography. Clinically significant disease was present in 75 patients, whereas 24 had no observable lesions and 2 had minimal lesions. Comparisons of individual lipid and lipoprotein levels were nearly all significantly different between patients with and patients without clinically significant disease; how ever, no single variable could predict the presence of disease among patients. Logistic regression analysis identified five factors: apolipoprotein A-I, apolipo protein B, diabetes, age, and family history of heart disease, which account for most of the differences between the two patient groups. These results could have important implications for the evaluation and management of patients sus pected of having coronary atherosclerosis.

Reversal of left ventricular intracavitary gradient with intracavitary diastolic regurgitation in hypertrophic obstructive cardiomyopathy

A 73 year old man presented with angina and nonsustained ventricular tachycardia. Cardiac catheterization revealed the dynamic systolic intracavitary gradient of hypertrophic obstructive cardiomyopathy. Abnormal isovolumetric relaxation resulted in the development of a diastolic gradient from the left ventricular outflow tract to the left ventricular apex accompanied by intracavitary regurgitation of contrast material from the outflow tract to the left ventricular body during left ventriculography. This case provides hemodynamic and angiographic confirmation of abnormal isovolumetric relaxation in this syndrome and insight into its mechanism.