Zakauddin Vera

Reversed Pulsus Paradoxus

Abstract The term reversed pulsus paradoxus may be used to describe an inspiratory rise of the arterial systolic and diastolic pressures, presumably related to an inspiratory increase in left ventricular stroke output. We have observed a reversed pulsus paradoxus in three unrelated clinical circumstances: idiopathic hypertrophic subaortic stenosis, isorhythmic ventricular rhythms and during intermittent inspiratory positive-pressure breathing in the presence of left ventricular failure. These unusual respiration-related fluctuations of blood pressure must be differentiated from the usual pulsus paradoxus of cardiac tamponade. (N Engl J Med 289:1272–1275, 1973)

Clinical pharmacology and therapeutic application of prazosin in acute and chronic refractory congestive heart failure: Balanced systemic venous and arterial dilation improving pulmonary congestion and cardiac output

Abstract The acute and chronic cardiocirculatory effects of the oral vasodilator, prazosin, were evaluated by cardiac catheterization, forearm plethysmography, echocardiography, treadmill exercise, and symptoms in nine patients with advanced long-standing congestive heart failure due to coronary disease. Oral prazsoin (2 to 7 mg) reduced forearm venous tone from 58.9 to 18.5 mm Hg/ml (p

Aberrancy of junctional escape beats. Evidence for origin in the fascicles of the left bundle branch.

Abstract The mechanism of aberrancy of so-called atrioventricular (A-V) Junctional escape beats was investigated in 8 cases, in 5 of which His bundle electrography was performed with both conducted and escape beats recorded. Aberrancy in Junctional beats usually shows features of incomplete or complete right bundle branch block and leftward or rightward shift of the QRS axis in the frontal plane. From the morphologic point of view the aberrancy resembles that seen in conducted beats with the additional feature of bifascicular block. Functional aberrancy based on incomplete recovery of the conduction fibers cannot account for aberrancy in slow Junctional rhythms. Phase 4 depolarization may explain the aberrancy in slow heart rates but cannot readily account for the fusion complexes so frequently seen in these rhythms. His bundle electrography in the present study showed a time relation between His spikes and the onset of the QRS complex which excludes the possibility of antegrade conduction of the aberrant beats along the same pathway used by descending sinus beats as well as true Junctional beats descending through the main His bundle. Specifically, the His spikes were found at or near the onset of the QRS complexes in aberrant escape beats, whereas they were ahead of the QRS complexes by the expected interval of 40 to 50 msec in the conducted beats. This temporal relation favors propagation of escape impulses from their origin bidirectionally, that is, simultaneously toward the ventricular myocardium and retrograde toward the main His bundle. This observation, together with the right bundle branch block and the axis deviation, places the escape focus in 1 of 2 fascicles of the left bundle branch: in the superior division for beats displaying right axis deviation and in the inferior division for beats displaying left axis deviation. With acceptance of a fascicular origin for these beats, a satisfactory explanation becomes readily available for the fusion complexes.

Left bundle branch block with intermittent right axis deviation. Evidence for left posterior hemiblock accompanying predivisional left bundle branch block.

Abstract A case of complete left bundle branch block with several episodes of intermittent marked right axis deviation is presented. All possible causes of the intermittent development of additional right axis deviation, such as electrolyte imbalances, lateral wall infarct, intermittent Wolff-Parkinson-White conduction, right bundle branch block, right ventricular hypertrophy and pulmonary embolism, were excluded. We conclude that the explanation for left bundle branch block with intermittent right axis deviation in our patient was the coexistence of left posterior hemiblock and predivisional left bundle branch block.

Recent advances in programmable pacemakers: Consideration of advantages, longevity and future expectations

The important electrical characteristics of conventional ventricular demand pacemakers currently widely employed are unable to be altered by noninvasive means after their implantation. However, a number of domestic pacemaker manufacturers have started to introduce a new modality for atraumatic modulation of these devices, the fully programmable pacemaker system, whereby the several variables regulating pacemaker operation may be optimized on an individual basis according to need. Such programmable pacemaker functions which can be varied include rate, energy output, refractory period and sensing threshold. The indications, significance and mechanisms for control of the various function programming are delineated for physician understanding at the present time.

Assessment of oral quinidine effects on sinus node function in sick sinus syndrome patients

The effects of therapeutic doses of orally administered quinidine sulfate on sinus rhythmicity and automaticity were observed in 11 patients with sick sinus syndrome (SSS). Evaluation of sinus node (SN) function was undertaken by assessing sinus nodal recovery time (SNRT), treadmill exercise testing, and 24-hour ambulatory ECG monitoring before and after quinidine administration (25 mg/kg) (range 800 to 1600 mg daily). Corrected SNRT ranged from 100 to 1320 msec (average 551) before quinidine and was not significantly (p greater than 0.05) altered after quinidine to 346 to 660 msec (average 481). Further, quinidine did not induce accelerated infrasinus pacemaker activity. Spontaneous sinus rate evaluated with ambulatory monitoring revealed average rate of 57 bpm (range 53 to 63) before quinidine without significant increase to average 59 bpm (range 52 to 80) after quinidine therapy. Similarly, the maximal SN response to exercise was not significantly affected by quinidine (average 129 bpm before and 129 bpm after drug therapy). It is concluded that therapeutic doses of quinidine do not exert adverse effects on SN function in SSS patients. Chronic oral quinidine therapy can therefore be used safely with caution in patients with chronic SN disease when indicated for control of tachyarrhythmias.

Clinical evaluation of the enhancement of vagal tone in acute myocardial infarction by edrophonium hydrochloride: Effects on ventricular arrhythmias, His bundle electrography, and left ventricular function

Enhanced electrical stability of acutely ischemic myocardium with vagal stimulation and acetylcholinesterase inhibition has been demonstrated experimentally. To extend these findings clinically, within 24 hours of acute myocardial infarction, 11 patients underwent continuous 10 hour Holter monitoring: 2.5 hour control before and after 5 hour constant edrophonium infusion (0.25 to 2.00 mg./minute). Continuous infusion of the agent lowered heart rate 92 to 78 b.p.m. (p less than 0.01). Although mean total ventricular extrasystoles (PVCs) per 5 hours per patient (131) and PVCs per 1,000 beats (4.7) were unchanged (p greater than 0.05), potentially lethal tachyarrhythmias (malignant PVCs: multifocal, R on T, paried, greater than 5 per minute or ventricular tachycardia) were terminated in six of 10 patients by edrophonium. However, serious ventricular arrhythmias continued in three patients and appeared in four despite the agent. Ventricular fibrillation did not occur during the 10 hour period of study. In addition, the patients were evaluated hemodynamically and by His bundle electrograms before and after a 10 mg. bolus of edrophonium prior to the 10 hour constant infusion: heart rate declined (88 to 72 b.p.m., p less than 0.01), while mean arterial pressure (98 mm. Hg), left ventricular filling pressure (14 mm. Hg), cardiac index (2.4 L. per minute per square meter), and stroke work index (36 Gm.m./M.2) were unchanged (p greater than 0.05). The edrophonium bolus prolonged the A-H interval (117 to 135 msec., p less than 0.01) while the H-Q interval was unaltered (48 msec; p greater than 0.05). It is concluded that increased vagal tone with edrophonium did not reduce the over-all presence of premature ventricular contractions in the entire study group; however, the malignant nature of PVCs and ventricular tachycardia appeared to be lessened by the parasympathomimetic agent in certain patients. In addition, no adverse hemodynamic or intraventricular conduction effects were produced by edrophonium administration.

Comparative evaluation of the efficacy of intravenous nitroglycerin and nitroprusside on reducing ventricular ischemia measured by vectorcardiographic-ST magnitude in experimental porcine myocardial infarction

COMPARATIVE EVALUATION OF THE EFFICACY OF INTRAVENOUS NITROGLYCERIN AND NITROPRUSSIDE ON REDUCING VENTRICULAR ISCHEMIA MEASURED BY VECTORCARDIOGRAPHIC-ST MAGNITUDE IN EXPERIMENTAL PORCINE MYOCARDIAL INFARCTION James M. Foerster, MD; Zakauddin Vera, MD; David Janzen, BS; Dean T. Mason, MD, FACC, Univ. of Calif., Davis, Calif. Controversy remains concerning clinical effects of nitroglycerin (NTG) and nitroprusside (NP) on extent of muscle damage with acute myocardial infarction (AMI). To evaluate influence of these two vasodilators on degree of such muscle injury, vectorcardiographic-ST magnitude rise (STM) was used to estimate myocardial ischemia that occurred with AM1 in the intact porcine heart, the coronary circulation of which is similar to man. Previously we have shown the Frank XYZ leads ST sum correlates closely with ST sum of multiple epicardial grid leads. In ten pigs, following thoracotomy and coronary ligature, the chest was closed and Frank XYZ leads obtained. Natural evolution of STM over 4 hours was observed in four animals, and in six pigs NTG and NP dose-responses were obtained following AMI. In pharmacologic treated animals, hemodynamics and STM were recorded 30-60 minutes after coronary ligation (pre-drug control) and then remeasured after either NTG or NP; each animal was used as its own control with time allowed between each drug for return of control hemodynamics. Control BP at LVFP at Min STM m LVFP Min STM Min STM attained NTG 103 22 76 21 +81% NP 109 26 82 17 +66% Min STM = minimum STM rise; p = mean blood pressure (mm Hg); LVFP = left ventricular filling pressure (mm Hg). These data indicate that both NTG and NP C ischemia extent in experimental AMI. Moreover, with 4 LVFP, NP appears more effective than NTG in + ischemia with AMI. ATTENUATION OF THE CARDIOVASCULAR EFFECTS OF NITROGLYCERIN BY INDOMETHACIN. Esteban Morcillo, M.D. Bertram Pitt, M.D. and Philip R. Reid, M.D. Johns Hopkins Medical Institutions, Baltimore, Maryland. An earlier report from this laboratory demonstrated that nitroglycerin (TNG) produced a marked increase in myocardial prostaglandins E release when given as a carstant infusion (IOk Kanu Chatterjee, MD, FACC; William Parmley, MD, FACC; Anne Norman, BA: University of California, San Francisco, California. Vasodilators have an established role in the therapy of heart failure. Recent studies have demonstrated hemodynamic improvement in chronic congestive heart failure with oral hydralazine and most recently oral prazosin. This study compares the hemadynamic effects of hydralazine (HD) and prazosin (PR) in the same patients with chronic heart failure. Changes in heart rate (HR), mean arterial pres8ure (MAP), pulmonary artery pressure. pulmonary capillary wedge pressure (PCW), right atria1 pressure, cardiac index (CI), stroke volume index (SVI), stroke work index (WI), systemic (SVR) and pulmonary vascular resistance were determined in 12 patients after 3. 4 and 5 mg of PR and compared to initial control hemodynamics (Cl). After second control hemodynamics (C2) the effects of 75 mg oral HD were determined in the same patients. The results were: MAP PCW CI SVI SW1 HR mHg mHg L/minim2 ml/m2 g *m/m2 SVR* Cl 86?7 07?3 24fl 2.1k.l 26?2 22t3 1776? 8.5 PR-5 mg 07+7 79+3 19?2 2.52.2 3023 25t3 141Ot118 C2 87f7 87?3 2421 2.12.1 2522 22t2 1760+ 86 HD 89f6 7922 2021 3.32.2 3823 3022 10452 60 PR increasedC1 by 19% and decreased SVR by 21%. while in these patients HD increaaedC1 by 52% and decreased SVR by 41%. There was no change in other hemodynamic parameters with either drug. Conclusion: These findings suggest that both PR and HD produce beneficial hemodynamic response and within prescribed doses, HD is twice as effective as PR.