Search PubMed⌕ Search

Biomedical subjects

Z Vera

Publications and source records attributed to Z Vera.

At least 19 recordsLinked to original sources
PubMed1991

Orthogonal electrode catheter array for mapping of endocardial focal site of ventricular activation.

Precise location of the endocardial site of origin of ventricular tachycardia may facilitate surgical and catheter ablation of this arrhythmia. The endocardial catheter mapping technique can locate the site of ventricular tachycardia within 4-8 cm2 of the earliest site recorded by the catheter. This report describes an orthogonal electrode catheter array (OECA) for mapping and radiofrequency ablation (RFA) of endocardial focal site of origin of a plunge electrode paced model of ventricular activation in dogs. The OECA is an 8 F five pole catheter with four peripheral electrodes and one central electrode (total surface area 0.8 cm2. In eight mongrel dogs, mapping was performed by arbitrarily dividing the left ventricle (LV) into four segments. Each segment was mapped with OECA to find the earliest segment. Bipolar and unipolar electrograms were obtained. The plunge electrode (not visible on fluoroscopy) site was identified by the earliest wave front arrival times of -30 msec or earlier at two or more electrodes (unipolar electrograms) with reference to the earliest recorded surface ECG (I, AVF, and V1). Validation of the proximity of the five electrodes of the OECA to the plunge electrode was performed by digital radiography and RFA. Pathological examination was performed to document the proximity of the OECA to the plunge electrode and also for the width, depth, and microscopic changes of the ablation. To find the segment with the earliest LV activation a total of 10 +/- 3 (mean +/- SD) positions were mapped. Mean arrival times at the two earlier electrodes were -39 +/- 4 msec and -35 +/- 3 msec. Digital radiography showed the plunge electrode to be within the area covered by all five electrodes in all eight dogs. The plunge electrode was within 1 cm2 area of the region of RFA in all eight dogs. The width and depth of ablation were 5 +/- 3.5 and 7 +/- 3.5 mm, respectively. Microscopic changes revealed coagulative necrosis, hemorrhage, and inflammatory changes in all RFAs. In conclusion, the OECA can map the endocardial focal site of origin of paced ventricular activation within 1 cm2 area in a canine model. RFA from the OECA can cause discrete ablations representing all five electrodes or cross-shaped ablation connecting central electrode to all four peripheral electrodes. This catheter holds promise for extending surgical and clinical catheter ablation procedures.

Animals↗
PubMed1991

Two phase radiofrequency catheter ablation of isolated ventricular endomyocardium.

UNLABELLED: This report describes a two phase radiofrequency (TPRF) energy source producing two radiofrequency sinusoidal voltages of similar frequency but different phase angles between three points of wire. When delivered through an orthogonal electrode catheter array (OECA) TPRF energy produces a square-shaped lesion of the area covered by the five electrodes (0.8 cm2). The purposes of the study were: to create square-shaped lesions using TPRF energy; to compare the size of lesions created by single phase radiofrequency (SPRF) to that of TPRF energy; and to study the depth of such lesions and to create lesions of desired size by adjacent placement of the OECA using TPRF energy. Ablations were created in nine isolated bovine hearts using three power settings (10, 20, and 40 watts) and three pulse durations (5, 10, and 20 seconds). Pathological examination was performed to document the length, width, depth, and the microscopic changes of ablations. TPRF energy increases the size of lesion (P less than 0.001) and utilizes less power (P less than 0.008) at the same power setting and pulse duration compared to SPRF energy. This is possibly related to earlier rise in impedance with TPRF compared to SPRF ablations. The largest lesion for both SPRF (0.51 +/- 0.08 cm2) and TPRF (1.03 +/- 0.18 cm2) ablations were observed at 20 watts for 20 seconds. By adjacent placement of the OECA and TPRF energy desired size (6 cm2) lesions were created. There was no significant difference between the depth of SPRF versus TPRF ablations at comparable power setting and pulse duration. Pathological examination revealed the shape of lesions were elliptical or cross-shaped for SPRF and square for TPRF ablations. Microscopic examination revealed coagulation necrosis, edema, and few necrotic cardiac muscle strands. CONCLUSIONS: TPRF energy can cause 1.2 cm2 lesions. TPRF compared to SPRF energy causes larger lesions but depth of lesions are not different than SPRF energy at the same power setting and pulse duration. By adjacent placement of OECA and TPRF energy desired size lesion can be created (6 cm2).

Animals↗
PubMed1991

Acute hypokalemia and inducibility of ventricular tachyarrhythmia in a nonischemic canine model.

Inducibility of sustained ventricular tachycardia (VT) and ventricular fibrillation (VF) by programmed ventricular stimulation following acute hypokalemia was studied in 21 anesthetized dogs free of inducible ventricular tachyarrhythmias at baseline. The control mean serum potassium concentration of 3.65 mEq/L was decreased to 2.14 mEq/L by insulin and furosemide administration. Inducibility of arrhythmias was also assessed following isoproterenol infusion before and after induction of hypokalemia. None of the animals developed sustained VT. Only one animal developed VF following hypokalemia (p greater than 0.05). Two normokalemic animals and five hypokalemic animals developed VF following isoproterenol infusion; this difference was not significant (p greater than 0.05). In this study, hypokalemia did not predispose to the development of a substrate necessary for the genesis and maintenance of VT. The inducibility of VF following hypokalemia was not significantly enhanced and appears to be related to the "aggressive" stimulation protocol.

Acute Disease↗
PubMed1990

Ventricular fibrillation following elective cardioversion in a patient with permanent pacemaker.

Elective cardioversion was undertaken in a patient with a VVI pacemaker and atrial tachyarrhythmia after converting the pacemaker to a VOO mode of function. The cardioverter output energy was unwittingly synchronized to the pacemaker output pulses that were falling randomly in various portions of the cardiac cycle. This resulted in the cardioverter DC shock being discharged in the ST segment of the native QRS with consequent ventricular fibrillation.

Aged↗
PubMed1986

Symptomatic and silent myocardial ischemia during exercise testing in coronary artery disease.

During exercise by patients with coronary artery disease (CAD), electrocardiographic evidence of myocardial ischemia may precede the onset of angina or may be unassociated with angina, even at peak levels of stress. However, neither the precise incidence of silent versus symptomatic ischemic episodes nor their interrelation in this setting has been clearly defined. The prevalence of silent and symptomatic myocardial ischemia during treadmill exercise testing was determined in 92 patients with angiographically documented CAD. The study group comprised 77 men (84%) and 15 women (16%) of mean age 57 years (range 32 to 79). Exercise testing resulted in ischemic ST-segment depression (greater than or equal to 1 mm for greater than or equal to 80 ms) only or in association with delayed (greater than or equal to 1 minute) angina in 39 patients (42%); angina only or in association with delayed ST-segment depression occurred in 42 patients (46%); and simultaneous occurrence of angina and ST-segment depression was noted in 11 patients (12%). Analysis of clinical, exercise and angiographic factors (age, sex, history of myocardial infarction, heart rate, maximal ST-segment depression, extent of CAD and left ventricular ejection fraction) revealed no significant correlation with the frequency of symptomatic and silent myocardial ischemia during exercise. Asymptomatic myocardial ischemia occurred commonly during exercise in patients with CAD, but there were no differences in the characteristics of patients with symptomatic and asymptomatic episodes.

Adult↗
PubMed1985

Accidental mediastinal entry via left internal jugular vein cannulation.

Two cases are reported in which mediastinal penetration by a pulmonary artery catheter and a temporary venous pacemaker wire occurred following cannulation of the left internal jugular vein and placement of an indwelling venous introducer sheath. The anatomy of the left internal jugular vein and possible mechanisms of accidental mediastinal penetration with this approach are discussed. Extreme caution must be exercised when using the left internal jugular venous access route and an indwelling venous introducer sheath.

Aged↗
PubMed1984

Electrocardiographic diagnosis of left ventricular hypertrophy in the presence of left bundle branch block.

The presence of left bundle branch block (LBBB) on 12-lead ECG may obscure the diagnosis of other ECG abnormalities including left ventricular hypertrophy (LVH). We retrospectively reviewed ECGs of patients with LBBB and LVH as determined by echocardiography to evaluate several ECG parameters as predictors of LVH. ECG evaluation included precordial voltage as measured by the sum of the S wave in leads V1 or V2 plus R wave in lead V6, QRS duration, mean frontal plane QRS axis, R wave amplitude in lead aVL, intrinsicoid deflection, and the presence or absence of criteria for left atrial enlargement. In the presence of LBBB and LVH, precordial voltage was significantly greater (p less than 0.001), QRS duration more prolonged (p less than 0.001), and left atrial enlargement more frequently present (p less than 0.001) than when LVH was not present. There was no difference in limb lead voltage, intrinsicoid deflection, or mean frontal plane QRS axis. Furthermore, the criterion of SV2 + RV6 greater than 4.5 mV demonstrated a sensitivity of 86% and a specificity of 100%. We conclude that a voltage criterion of SV2 + RV6 greater than 4.5 mV is diagnostic of LVH in the presence of LBBB; furthermore, QRS duration of greater than 160 msec plus left atrial enlargement strongly supports the diagnosis of LVH.

Bundle-Branch Block↗
PubMed1982

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.

Administration, Oral↗
PubMed1982

Cardiocirculatory actions of trimazosin and sodium nitroprusside in ischemic heart disease.

Although postload-reducing drugs are effective vasodilators in chronic congestive heart failure, the clinical application of the approach to ambulatory patient management remains difficult. We compared the hemodynamic effects of the new oral systemic vasodilator trimazosin (TZ) with those of nitroprusside (NP). Both TZ (172 mg) and NP (46 microgram/min) decreased mean blood pressure modestly (P less than 0.001), while causing considerable decline in elevated left ventricular filling pressure (TZ from 30 to 24 mm Hg; NP from 31 to 20 mm Hg; both P less than 0.001). TZ also raised the low cardiac index (CI) of 2.02 to 2.59 1/min/M2 (P less than 0.001), whereas NP elevated CI from 2.16 to 2.96 1/min/M2 (P less than 0.001). Both drugs lowered (P less than 0.05) total systemic vascular resistance and pressure time/minute while enhancing (P less than 0.01) stroke work index. The drugs diminished forearm venous tone (P less than 0.02) and forearm vascular resistance (P less than 0.01) concomitantly with elevation of forearm blood flow (P less than 0.05). Thus, TZ induced qualitatively similar marked augmentation of cardiac function to that by NP. These encouraging hemodynamic findings indicate that TZ may be beneficial to patients undergoing ambulatory vasodilator therapy of severe chronic congestive heart failure.

Adult↗
PubMed1979

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.

Arrhythmias, Cardiac↗
PubMed1978

Effects of digitalis on sinus nodal function in patients with sick sinus syndrome.

The effect on sinus rhythmicity and automaticity of complete digitalization in a 24 hour period was observed in 14 patients with sick sinus syndrome. Sinus nodal function was evaluated in these patients by assessing sinus nodal recovery time and by treadmill exercise testing and 24 hour Holter monitoring, before and after digoxin administration. Corrected sinus nodal recovery times ranged from 240 to 2,065 msec (average 714) before digoxin and were shortened to 250 to 1,260 msec (average 565) after the glycoside. Further, digoxin induced accelerated infra sinus escape pacemaker activity in five patients: junctional and ventricular in one and atrial in four. Spontaneous sinus rate evaluated with Holter monitoring revealed an average of 56 beats/min (range 43 to 69) before digitalis that was unchanged (average 58 beats/min; range 48 to 74) after digoxin therapy. Similarly, the sinus nodal response to exercise was unaffected after digitalization (average 118 beats/min both before and during digitalis therapy). It is concluded that digoxin does not exert adverse effects on sinus nodal function in patients with sick sinus syndrome. The glycoside can be used safely in these patients when indicated for cardiac pump dysfunction or for control of tachyarrhythmia.

Adult↗
PubMed1977

Identification of sudden death risk factors in acute and chronic coronary artery disease.

Because of their potential role in the pathogenesis of sudden death, cardiac arrhythmias in patients with coronary artery disease have become the subject of increasing concern and investigation. A series of studies on the problem of ventricular ectopy as it relates to the entire spectrum of sudden death in coronary disease were carried out utilizing continuous portable electrocardiographic monitoring systems. Evaluation of arrthymias during the entire 3 week in-hospital period after acute myocardial infarction in 83 patients revealed that absence of premature ventricular contractions, including their serious forms (multifocal, paired, R on T phenomenon, frequency 5/min or greater) and ventricular tachycardia in the coronary care unit did not exclude their high incidence rate (premature ventricular contractions 30 percent, serious forms 41 percent, ventricular tachycardia 6 percent) in the late hospital phase. Because late hospital serious forms of ventricular ectopy correlated with arterial hypoxia and elevated left ventricular filling pressure in the coronary care unit and with persistent S-T abnormalities, the extent of left ventricular dysfunction and ischemia with acute myocardial infarction appeared precursors to these arrhythmias. Study of ventricular ectopy in the late hospital phase of acute myocardial infarction indicated that ventricular ectopy and particularly its serious forms and prognostic significance relative to subsequent sudden death after discharge; the extent of predischarge S-T segment alterations was greater in subjects who died suddenly than in survivors, suggesting that persistent ischemia or segmental dyssynergy, or both, predisposed to lethal arrhythmias. Among 86 patients with chronic coronary disease documented by catheterizerization, 87 percent had ventricular ectopy and 62 percent serious ventricular arrhythmias, in contrast to 34 percent and 9 percent, respectively in normal subjects; frequency of serious forms of ventricular ectopy was related to extent of coronary atherosclerosis. Correlation of standard electrocardiograms with continuous Holter electrocardiograms in 101 patients with chronic coronary disease over 24 months revealed that the former modality was insensitive in arrhythmia detection; patients free of ventricular ectopy by serial standard electrocardiograms had a 62 percent incidence rate of serious forms of ventricular ectopy and 6 percent ventricular tachycardia on portable continuous monitoring. Additional studies of patients with chronic coronary disease showed that assessment of both the type of ventricular ectopy and the setting in which it occurs provides the most meaningful characterization of risk of sudden death. These systematic series of observations identify premature ventricular ectopic beats as important and separate risk factors in coronary disease...

Acute Disease↗
PubMed1977

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 (PVC's) per 5 hours per patient (131) and PVC's per 1,000 beats (4.7) were unchanged (p greater than 0.05), potentially lethal tachyarrhythmias (malignant PVC's: 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.

Acetylcholinesterase↗
PubMed1977

Efficacy of disopyramide phosphate in the treatment of refractory ventricular tachycardia.

The effects of intravenously administered disopyramide phosphate were evaluated in seven patients with refractory ventricular tachycardia. All patients had organic heart disease, including acute infarction (three patients), chronic coronary artery disease (two patients) and cardiomyopathy (two patients). The severity of the heart disease was reflected in the advanced patient age (average 64 years) and the occurrence before disopyramide therapy of cardiac arrest in five patients and congestive heart failure in all seven patients. In five patients, disopyramide was given as a bolus injection, 2 mg/kg body weight, followed by an infusion of 20 to 40 mg/hour. The final two patients received 4 mg/kg divided as a bolus injection and an infusion over 1 hour followed by a 0.4 mg/kg infusion during the next hour. Intravenous administration of disopyramide resulted in more effective electrical stability in all patients and completely eliminated ventricular tachycardia in six. Recurrence of ventricular tachycardia was prevented in six patients with subsequent long-term oral administration of disopyramide. Possible dose-related cardiac pump depression occurred in two patients, but disopyramide was otherwise well tolerated. Therefore, these data document the therapeutic efficacy of disopyramide in the treatment of refractory life-threatening ventricular tachyarrhythmias.

Aged↗