Search PubMed⌕ Search

Biomedical subjects

Z Vera

Publications and source records attributed to Z Vera.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1977

Improvement of symptoms in patients with sick sinus syndrome by spontaneous development of stable atrial fibrillation.

Fifty-six patients with symptomatic chronic sinus bradycardia because of sick sinus syndrome (SSS) were followed for periods from one month to 11 years (average 3-2 years). Eleven developed stable atrial fibrillation persisting for 8 to 61 months; 52 had permanent demand pacemakers implanted before atrial fibrillation commenced. In the 11 patients with atrial fibrillation, 10 had adequate ventricular rate, 8 with rates greater than 100 beats/min requiring digoxin for rate control. The 8 patients with atrial fibrillation with pacemakers remained asymptomatic for 13 to 18 months without requiring reimplantation; battery failure occurred in 2 whose rapid ventricular rates were controlled by digoxin. In the other 6 patients with pacemakers who developed atrial fibrillation, adequate ventricular rates persisted resulting in overdrive suppression. No patient had systemic embolisation. The previous duration of symptomatic sinus bradycardia was longer in patients developing atrial fibrillation (average 5-5 years) compared (P less than 0-01) with patients without atrial fibrillation (1-9 years). Further, premature atrial contractions occurred in all 11 patients before atrial fibrillation in contrast to only 21 of the 45 patients without atrial fibrillation. It is concluded that occurrence of atrial fibrillation in SSS with symptomatic sinus bradycardia provides a natural cure of symptoms caused by bradycardia. These data indicate that permanent ventricular pacing may not be necessary if persistent atrial fibrillation develops in SSS.

Aged↗
PubMed1977

Evaluation of precordial orthogonal vectorcardiographic lead ST-segment magnitude in the assessment of myocardial ischemic injury.

Relationship has been established between epicardial ST-segment elevation, considered a reliable estimate of ischemic injury in experimental myocardial damage, and ST changes by multiple-lead precordial electrocardiography. However, 35-lead precordial mapping is time-consuming and suitable only for anterior infarctions. An alternate, more rapid method for recording ST segments is an external 3-lead orthogonal vectorcardiographic (VCG) system which also can assess the entire ventricle. Accordingly, validity of VCG ST magnitude was evaluated by direct comparison with changes in epicardial ST magnitude (EST) induced by occlusion of major coronary arteries, reperfusion, and pharmacologic interventions in 15 closed-chest dogs. A total of 404 data points (average 27/dog), 20 epicardial grid and 3 Frank XYZ leds each, demonstrated close correlation (least squares linear regression) between VCG ST and EST changes (r = 0.921 +/- 0.02 SEM). These data document the accuracy of precordial VCG ST in noninvasive assessment of ischemic injury in various areas of myocardium and its practicality for clinical application.

Animals↗
PubMed1977

Noninvasive assessment of cardiac function and ventricular dyssynergy by precordial Q wave mapping in anterior myocardial infarction.

To determine whether multiple lead precordial electrocardiographic recordings offer an improved index for noninvasive estimation of left ventricular hemodynamic function and segmental dyssynergy, precordial mapping was performed in patients with anterior myocardial infarction, and the number of pathologic Q waves (greater than or equal to 0.04 sec) was counted (Q-Index). Left ventricular function was determined by cardiac catheterization and angiography and correlated with the Q-Index. The Q-Index correlated well with dyssynergy extent (r = 0.84) and inversely with ejection fraction (r= -0.87), stroke work index (r = -0.79) and cardiac index (r = =0.66). Three patient groups were defined by Q-Index; group I, 0.04 sec Q complexes less than 15; group II, 15-25; group III, 26-35. Q-Index related closely to functional classification and survival (mean follow-up 12.2 months): group I, 91%; group II, 81%; group III, 40%. Thus 35-lead precordial Q wave mapping with determination of total number of pathologic Q waves permits practical, atraumatic assessment of hemodynamic and functional status and allows prediction of survival in acute and chronic anterior myocardial infarction.

Adult↗
PubMed1977

Electrocardiographic response to intravenous urography: prospective evaluation of 275 patients.

A total of 275 consecutive patients referred for intravenous urography were monitored for electrocardiographic changes during administration of Conray 400 or Renovist II in the form of either intravenous bolus or infusion. Three patients who received Conray (two bolus and one infusion) developed sustained ventricular tachycardia; they reverted to sinus rhythm with intravenous lidocaine. A statistically significant (P less than .05) number of patients developed a heart rate increase of 10 beats/min or more with bolus of either drug (65 of 128) compared to infusion (21 of 147). Depression of ST segment (greater than or equal to 0.5 mm) was encountered statistically more often (P less than .05) with bolus (20 of 128) compared to infusion (six of 147). Increase of corrected QT of 0.10 sec or more was observed more often (P less than .05) with bolus (43 of 128) compared to infusion (five of 147). Abnormal resting ECG, coronary artery disease, or congestive heart failure imposed a higher (P less than .05) risk for development of ventricular tachycardia, ST depression, or ectopic ventricular beats. It is concluded that a bolus injection be very cautiously administered to patients with risk factors such as abnormal ECG, coronary artery disease, or congestive heart failure during intravenous urography and that resuscitative facilities be available.

Adolescent↗
PubMed1976

Reduction of S-T segment elevation with infusion of nitroprusside in patients with acute myocardial infarction.

The effect of infusion of sodium nitroprusside on S-T segment elevation was evaluated in 12 patients with acute anterior myocardial infarction. Precordial 35 lead S-T segment maps were obtained in each patient immediately before and 10 minutes after infusion of 53 mug/min (range 20 to 100 mug/min) of nitroprusside. The following measurements were made from each S-T map: sigmaST (total S-T elevation in all leads), NST (number of leads with S-T elevation greater than 1 mm) and ST (average (S-T elevation in leads with more than 1 mm elevation). After administration of mitroprusside, evidence of myocardial ischemic injury as assessed by S-T mapping decreased in association with reduction of the myocardial oxygen consumption index of pressure-time per minute. Group mean values diminished significantly for sigmaST (41.7 to 28.6 mm, P less than 0.001), NST (20.3 to 14.6, P less than 0.001) and ST (1.6 to 1.2 mm, P less than 0.005). Pressure-time per minute decreased from 2,690 to 2,372 mm Hg-sec/min (P less than 0.001). Because there was no significant relation (P less than 0.05) between reductions in S-T elevation and lower indexes of myocardial oxygen consumption, it is suggested that nitroprusside may possess a separate action of augmenting regional blood flow to ischemic myocardium. Evaluation with the precordial S-T mapping technique suggested that intravenous administration of nitroprusside was associated with evidence of reduced ventricular ischemic injury in patients with acute myocardial infarction. This effect appears to be related to reduction of myocardial oxygen demand by the peripheral cardiac unloading mechanisms of nitroprusside as well as to a possible direct action of the drug in improving regional blood flow to ischemic heart muscle.

Acute Disease↗
PubMed1976

Prolonged His-Q interval in chronic bifascicular block. Relation to impending complete heart block.

Although prolonged infra-His conduction time in bifascicular block is suspected of denoting trifascicular disease, adquate documentation is lacking concerning the correlation between lengthened His-Q interval (H-Q) and the risk of development of complete heart block (CHB). H-Q in conducted sinus beats in patients with bifascicular block associated with Mobitz II or intermittent CHB represents the approximation of maximal H-Q prolongation prior to onset of trifascicular block. To assess this relationship between prolongation of H-Q and trifascicular block, His bundle electrocardiography (HBE) was performed in 50 patients with chronic bifascicular block exhibiting Mobitz II block or transient CHB. Mobitz II or episodic CHB was shown in all patients: within two days prior to HBE in 45/50 patients; in 39/50 patients during HBE; and following HBE in five patients. In 49/50 patients H-Q was prolonged (greater than 55 msec) and in 47 this interval was substantially lengthened (65 msec or greater). Since marked H-Q prolongation in conducted sinus beats was documented in nearly all patients with bifascicular block associated with intermittent complete trifascicular block, we conclude that a considerably lengthened H-Q interval in bifascicular block is not only a usual prerequisite but strong evidence, for impending complete heart block.

Adult↗
PubMed1976

Alterations in ventricular contraction pattern in the Wolff-Parkinson-White syndrome. Detection by echocardiography.

The effects of abnormal ventricular activation upon the contractile pattern of the ventricles in patients with the Wolff-Parkinson-White syndrome (WPW) remain uncertain. Therefore we compared the motion of the anterior right ventricular wall (RV), the interventricular septum (IVS), and left ventricular posterior wall (LVPW) on echogram in nine patients with WPW and one patient with a coronary sinus pacemaker (CSP) to 20 normal subjects. Normal subjects manifested posterior RV motion which began and reached maximal excursion at 175 and 366 msec (group mean), respectively, after the onset of the QRS complex; posterior movement of the IVS which started and peaked at 90 and 30 msec, respectively; and anterior contraction of the LVPW which began and peaked at 159 and 406 msec, respectively. Five of seven patients with Type A WPW demonstrated a localized area of premature contraction of the LVPW occuring during the initial 100 msec interval following the onset of the QRS complex which was accompanied by paradoxic anterior motion of the IVS. Thereby in Type A patients initial and maximal posterior motion of the IVS occurred later, 230 (P less than 0.001) and 400 (P less than 0.05) msec, and anterior motion of the LVPW occurred earlier, 75 (P less than 0.001) and 367 (P less than 0.05) msec as compared to normal. The amplitude and duration of early contraction could be related to the prominence of the delta wave during atrial pacing. Similar premature contraction was also observed in the patient with CSP during paced beats. One Type B WPW patient exhibited abnormal IVS motion while the additional patient manifested premature LVPW contraction similat to that seen in Type A patients. The contractile pattern of the right ventricular anterior wall was recorded in five of seven Type A Wolff-Parkinson-White patients and manifested prolongation of the interval from the onset of the QRS complex to the initial posterior movement (group mean 234 msec, P less than 0.05) as compared to normal. Thus echocardiography can be used to confirm the diagnosis and to improve understanding of the pathophysiology of the Wolff-Parkinson-White syndrome.

Adolescent↗
PubMed1976

Reduction of ischemic injury by sublingual nitroglycerin in patients with acute myocardial infarction.

The effect of sublingual nitroglycerin (NTG) on myocardial ischemic injury was evaluated in eleven patients with acute anterior myocardial infarction. Precordial 35-lead ST-segment maps were obtained in each patient immediately before and 3-10 minutes after 0.4 mg sublingual NTG. The following measurements were made from each ST map: N-ST (number of leads showing ST elevation greater than 1mm), sigmaST (total ST elevation in all leads), ST (average ST-segment elevation in those leads with less than 1mm elevation). Following 0.4 mg sublingual NTG evidence of myocardial ischemic injury as assessed by ST-segment mapping decreased in association with reduction of heart rate X systolic blood pressure product (10.80 X 10(3) to 9.49 X 10(3), P less than 0.001). Group mean values diminished significantly for N-ST (18.1 to 14.4, P less than 0.001), sigma ST (37.9 to 30.1 P less than 0.005) and ST (1.7 to 1.4, P less than 0.001). Evaluation performed by the technique of precordial ST-segment mapping suggests that sublingual nitroglycerin in a commonly employed clinical dose is associated with evidence of reduced ischemic cardiac injury in patients with acute myocardial infarction. This effect appears to be related to reduction of myocardial oxygen demand by the nitrate.

Acute Disease↗
PubMed1976

Intraventricular free wall dissection causing acute interventricular communication with intact septum in myocardial infarction.

This report delineates a previously unrecognized complication of acute myocardial infarction, an intraventricular wall dissection producing interventricular communication without septal perforation. The clinical, hemodynamic, and pathologic features of this unique condition are documented, as well as the factors important in the mechanism of its production.

Aged↗
PubMed1976

Rapid overdrive pacing of refractory tachyarrhythmias in patients after open-heart surgery.

The efficacy of rapid ventricular pacemaker overdrive in the treatment of supraventricular and ventricular tachyarrhythmias is presented as a new approach to the management of these rhythm disorders inpatients after cardiac surgery. This mode of therapy is exemplified in the control of heart rate and return of normal sinus rhythm in patients with both types of tachyarrhythmias refractory to conventional antiarrhythmic agents. In addition, the pathogenesis and mechanisms of pacemaker overdrive in termination these rhythm disturbances are delineated.

Bundle-Branch Block↗
PubMed1975

Electrophysiologic properties of perhexiline.

Perhexiline maleate (Pexid), a promising clinical antiarrhythmic and antianginal drug, was evaluated for its electrophysiologic effects on the entire conduction system of the intact canine heart throughout a wide range of therapeutic and potentially toxic doses. Intracardiac conduction times were measured by bipolar intramyocardial and transvenous endocardial electrodes before and following the intravenous administration of each dose of perhexiline maleate, 3 mg/kg every 30 min for a total of 4 doses in 7 open-chest anesthetized dogs. Eight animals served as controls in which similar operative technique and electrophysiologic variables were recorded after infusion of the maleate diluent. In addition, the effects of perhexiline on atrial and ventricular thresholds to electrical stimulation were recorded, as well as the QRS and QT intervals, sinus rate, and rhythm disorders. It was observed that perhexiline did not significantly (p greater than .05) alter sinus rate, QT interval, QRS duration, PR interval, intra-atrial conduction time, atrioventricular nodal conduction time, and His-Purkinje conduction velocity. The drug did not affect the cardiac threshold to electrical stimulation of less than 0.1 ma. No ectopic atrial or ventricular activity emerged during the accumulated influence of the agent. From this study, it is concluded that perhexiline does not exert deleterious actions on the conduction system of the intact canine heart. In view of the negligible toxic effects and its efficacy in treating ventricular tachyarrhythmias in patients, the drug deserves further clinical evaluation.

Animals↗
PubMed1975

Lack of sensing by demand pacemakers due to intraventricular conduction defects.

A previously unrecognized form of failure of normally functioning noncompetitive R-inhibited or R-triggered pacemakers to sense is described in 30 patients. The failure was produced by the delayed arrival of ventricular depolarization due to intraventricular conduction disturbances at the site of pacemaker sensing electrodes. These patinets with late activation of the right ventricle exhibited right bundle branch block (RBBB) during conducted sinus beats or had ectopic beats arising from the left ventricle. In both these situations, several late occurring QRS complexes were not sensed by the pacemaker electrodes in the right ventricular apex (RVA) and thereby the R-inhibited pacemaker spike discharged into the initial portion of the QRS complex. Activation of the RVA was delayed up to 65 msec in sinus beats with RBBB and even longer in premature beats arising from the left ventricle. The depolarization front of such beats reached the myocardium around the right ventricular pacemaker electrodes late in the QRS and thereby were not sensed up to 65 msec after the QRS onset as seen on the surface electrocardiogram (ECG). It was found in this study that if the inscription of such QRS complexes began up to 65 msec before the next due pacemaker impulse, these complexes were not sensed, allowing discharge of normally functioning R-inhibited pacemakers within the QRS which mimicked pacemaker malfunction. Failure to sense due to this phenomenon was observed in patients with noncompetitive pacemakers, both R-inhibited and R-triggered; temporary and permanent; with unipolar as well as bipolar electrodes. Similarly, patients with left ventricular epicardial electrodes and left bundle branch block in sinus beats also exhibited this phenomenon. Complete evaluation proved that pacemaker function was normal in the entire patient group. Recognition that failure to sense was the result of intraventricular conduction disorder prevented the untimely replacement of the pulse generator. This phenomenon of nonsensing by noncompetitive pacemakers should be considered in the presence of wide QRS complexes before the pacemaker is concluded to be malfunctioning.

Aged↗