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Biomedical subjects

K M Kessler

Publications and source records attributed to K M Kessler.

At least 109 records · Page 6Linked to original sources
PubMed1987

Pharmacologic approaches to management of arrhythmias in patients with cardiomyopathy and heart failure.

Interactions between disordered cardiac rhythm and abnormal cardiac hemodynamic function are well recognized. Demonstrations of this relationship include the relationship between prognostic significance of ventricular ectopy and left ventricular ejection fraction, impairment of ventricular function in association with loss of atrial systole in disease states, increased risk of potentially lethal arrhythmias in the myopathic ventricle, and the evolution of advanced grades of ventricular arrhythmias in acute heart failure. With the development of newer and more potent antiarrhythmic agents, in conjunction with drugs that can improve the failing circulation, it is now possible to clarify these interrelationships and perhaps develop new strategies for clinical management.

Anti-Arrhythmia Agents↗
PubMed1987

Clinical parameters of adolescent Hispanic male hypertensive subjects: a new subject?

We have previously reported an increased prevalence of elevated blood pressure in Hispanic adolescent males. The pressure elevation did not correlate with weight. In this study, we evaluated the response to antihypertensive therapy of eight adolescent Hispanic males found to have elevated pressure during high school screening. All patients were placed on placebo tablets b.i.d. for 2 weeks with weekly blood pressure readings. Those with persistently elevated pressures (at or above the 95th percentile) underwent laboratory testing, exercise testing, and echocardiography. An age-matched group of Hispanic adolescents with blood pressure recording below the 90th percentile were also exercised. Patients were then placed on 0.1 mg clonidine b.i.d. for 12 weeks. Pretherapy exercise testing demonstrated an abnormal systolic hypertensive response (mean 193 +/- 43 mmHg) that improved after therapy (mean 167 +/- 28 mmHg). Echocardiographic data were normal. All patients had elevated levels of VLDL and triglycerides. Five patients also had HDL levels below the 50th percentile for age and sex. We conclude that this population is similar to other hypertensive adolescent populations in exercise response pre- and posttherapy with clonidine, but they demonstrated a unique clinical feature in the elevation of the VLDL and triglyceride lipoprotein fractions.

Adolescent↗
PubMed1986

Cardiovascular findings in quadriplegic and paraplegic patients and in normal subjects.

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/m2, p less than 0.01) compared with normal volunteers (102 +/- 16 g/m2) or paraplegic patients (110 +/- 26 g/m2). 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 degrees vs 42 +/- 41 degrees, p less than 0.005) and smaller left atrial dimensions (2.4 +/- 0.4 vs 3.0 +/- 0.3 cm, p less than 0.005). The quadriplegic group was characterized by a significantly reduced mean blood pressure (67 +/- 7 vs 88 +/- 8 mm Hg in normal subjects, p less than 0.002), high normal peripheral resistances (22 +/- 5 vs 17 +/- 5 units in normal subjects, difference not significant) and a markedly reduced calculated cardiac output (3.2 +/- 0.6 vs 5.4 +/- 1.4 liters/min in normal subjects, p less than 0.01). Hemodynamic data for the paraplegic patients were similar to those in the normal group. A decrease in LV wall stress, mediated primarily by a decrease in venous return, appeared to result in the "adaptive" cardiac atrophy seen in these quadriplegic patients. LV asynergy was common and also may be related to a decrease in cardiac filling.

Adolescent↗
PubMed1986

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.

Angiography↗
PubMed1986

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.

Aged↗
PubMed1986

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.

Aged↗
PubMed1985

Mitral valve alternans.

An echogram showing mitral valve alternans was recorded in a patient with advanced cardiomyopathy and pulsus alternans induced by premature ventricular depolarizations. Decreased left ventricular emptying by the weak beat was followed by blunting of the subsequent mitral valve E point, a finding compatible with a significant elevation of left ventricular pressure in early diastole. Both alternating systolic (contractile state) and diastolic (pressure and dimension) variables seemed to participate in the alternans phenomenon in this patient.

Arrhythmias, Cardiac↗