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Biomedical subjects

B Strasberg

Publications and source records attributed to B Strasberg.

At least 127 records · Page 7Linked to original sources

Alternating Wenckebach periods in acute inferior myocardial infarction: clinical, electrocardiographic, and therapeutic characterization.

We report on twelve patients with alternating Wenckebach periods (AWP) occurring during an acute inferior myocardial infarction (AIMI). There were nine males and three females, with a mean age of 61 years (range, 43 to 75). AWP appeared during the first 48 hours of the AIMI in 10 patients and on the fourth day of hospitalization in two patients. AWP occurred spontaneously in nine patients and following the administration of atropine in the remaining three patients. Mean systolic blood pressure significantly decreased during AWP as compared to the period preceding or following the bradyarrhythmia (93 +/- 42 mmHg vs 123 +/- 37 mmHg, p less than 0.02). Killip functional class was significantly higher during AWP as compared to the period preceding or following the bradyarrhythmia (2.1 +/- 1.2 vs 1.5 +/- 0.8, p less than 0.02). Pacemaker therapy was initiated prophylactically in two patients, because of syncope in six, because of hemodynamic deterioration in two, and for syncope and hemodynamic deterioration in two. Three patients died in cardiogenic shock despite pacemaker therapy. No evidence of right ventricular infarction was seen in the patients. Atropine administration during AWP significantly increased the sinus rate and significantly decreased the ventricular rates and the systolic blood pressure. In addition, three patients developed long bouts of paroxysmal AV block. Isoproterenol administration improved AV conduction in one patient, caused no change in two patients and induced non-sustained ventricular tachycardia in three patients. In conclusion, AWP occurring during AIMI is a symptomatic bradyarrhythmia associated with hemodynamic deterioration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Polymorphous ventricular tachycardia and atrioventricular block.

Nine patients are presented who had polymorphous ventricular tachycardia (PMVT) occurring during atrioventricular (AV) block. There were five men and four women with a mean age of 80 +/- 9 years. Five patients had organic heart disease and the remaining four had primary conduction disease (bundle branch block). AV block was complete in four patients (2:1 in three, and paroxysmal in two). The mean ventricular cycle length (of the AV block rhythm) was 1567 +/- 203 ms. The mean QT interval was 0.64 +/- 0.09 s and the mean QTc was 0.51 +/- 0.06 s. When compared to a similar control group with AV block but without PMVT, the ventricular cycle length was similar but the QT and QTc were significantly longer. PMVT was usually of short duration (eight beats to 12 s) and in seven of these nine patients, frequent premature ventricular beats (PVBs) were recorded at various times from the occurrence of PMVT. This is in contrast to the control patients in whom PVBs were detected in one patient only. In conclusion, patients with AV block who develop PMVT usually have longer QT intervals and have detectable PVBs on routine ECGs, unlike similar patients with AV block but without PMVT. In a patient with AV block, a QT interval above 0.60 s and PVBs on the ECG seem to indicate an increased risk for the development of PMVT.

Aged↗

Efficacy of intravenous amiodarone in the management of paroxysmal or new atrial fibrillation with fast ventricular response.

We tested the efficacy of intravenous amiodarone (5 mg/kg) in slowing ventricular response and/or restoring sinus rhythm in 26 patients with paroxysmal or new atrial fibrillation with fast ventricular response. There were 16 men and 10 women with ages ranging from 35 to 84 years, mean 63 years. Intravenous amiodarone initially slowed the ventricular response in all patients from 143 +/- 27 to 96 +/- 10 beats/min (P less than 0.001). Twelve patients (46%) reverted to sinus rhythm within the first 30 min (range 5 to 30 min, mean 14 +/- 9 min). One patient reverted to atrial flutter after 10 min and 40 min later to sinus rhythm. Six patients (23%) converted to sinus rhythm after 2 to 8 hr and in these 6 cases, the initial slowing in ventricular response obtained with amiodarone persisted until conversion. Seven patients (27%) did not convert to sinus rhythm following amiodarone administration and they required further medical therapy to slow the ventricular response and/or to convert to sinus rhythm. No serious side effects from drug administration were noted. Intravenous amiodarone appears as a highly effective medication in the conversion or control of new onset atrial fibrillation with fast ventricular response.

Adult↗

Amiodarone-induced sinoatrial block.

We observed sinoatrial block due to chronic amiodarone administration in a 5-year-old boy with primary cardiomyopathy, Wolff-Parkinson-White syndrome and supraventricular tachycardia. Reduction in the dosage of amiodarone resulted in the disappearance of the sinoatrial block and the persistence of asymptomatic sinus bradycardia.

Amiodarone↗

Right ventricular dysfunction in acute inferoposterior myocardial infarction. An echocardiographic and isotopic study.

We analyzed right ventricular (RV) regional wall motion by two-dimensional echocardiographic (2D echo) and multigated acquisition radionuclear (MUGA) studies in 104 patients with acute inferoposterior myocardial infarction (AIPMI). Sixty-eight patients (65 percent) had 2D echo RV regional wall motion abnormalities (RV dysfunction(RVD) group) while 36 patients showed no 2-D echo RV regional wall motion abnormalities (no-RVD group). The RVD group had a higher incidence of jugular venous engorgement (p less than 0.05), Kusmaul's sign, (p less than 0.05) complete atrio-ventricular block (p less than 0.05), and in-hospital death (p less than 0.02). The RVD group had significantly higher 2-D echo RV end-systolic dimensions (p less than 0.005) and lower values of percentage of fractional shortening (%FS) (p less than 0.005) in the long and short axis of the RV four-chamber view than patients in the no-RVD group and a control group of 20 patients with normal hearts. There was no statistical significant difference in the 2-D echo RV end-diastolic dimensions among the three groups. Patients in the RVD group had a lower MUGA derived RV ejection fraction (EF) than patients in the no-RVD and control groups (26.5 +/- 13.2 vs. 46.3 +/- 7 and vs. 50.6 +/- 4, respectively; p less than 0.05). RVD was diagnosed by both 2-D echo and MUGA in 60 of 104 patients (57.7 percent) with a sensitivity for 2-D echo of 92 percent and 79 percent specificity (when compared to the MUGA study). The predictive value for a positive test was 88 percent and for a negative test 86 percent. The accuracy was 87.5 percent. Recognition of regional wall motion abnormalities by 2-D echo permits a prompt and accurate bedside identification of right ventricular dysfunction (RVD) within the first 72 hours of clinical onset. An enlarged RV 2D echo end-diastolic dimension was not a sensitive parameter for the diagnosis of this pathology, whereas an increased end-systolic RV diameter and decreased RV %FS were better indicators of RV dysfunction in patients with acute inferoposterior wall myocardial infarction.

Aged↗

A simplified QRS scoring system for the estimation of the severity of acute inferior wall myocardial infarction.

Electrocardiographic assessment of the R/Q wave ratio (lead 2) of patients with a first acute inferior wall myocardial infarction (IWMI) offers important indirect quantitative information regarding the severity and extent of the myocardial damage. Eighty-eight consecutive patients with IWMI were investigated by echocardiography and radionuclear angiography. After measuring the R/Q ratio in lead 2 during the ST-wave stabilized stage of myocardial infarction, patients were separated into three groups--group 1 with an R/Q ratio greater than 2; group 2 with an R/Q ratio between 1 to 2; and group 3 with an R/Q ratio less than 1. Utilizing the information thus gathered from the electrocardiogram (ECG) offers a simple and efficient method for early prognosis which merits further investigation.

Adult↗

Polymyositic heart disease.

There is an apparent correlation between the severity and duration of skeletal muscle involvement, cardiac manifestations and the extent of conduction system disease in polymyositis. Cardiac involvement during the course of polymyositis has been recognized as one of the typical features of skeletal muscle myositis. We report a patient with polymyositis in whom bifascicular block, prolonged P-R interval and congestive heart failure appeared three years before any clinical or laboratory evidence of active skeletal muscle myositis. To the best of our knowledge, this is the first report of polymyositis where cardiac manifestations preceded those of skeletal muscle myositis.

Cardiomyopathies↗

Use of the Shaw Scalpel in pacemaker operations.

Pacemaker carriers are at risk when undergoing operations involving the use of diathermy. The Shaw Scalpel utilizes a method by which the cutting edge of the blade is heated to a selected temperature that seals blood vessels as they are cut. No electrical currents are passed to or through the patient and there is no sparking or electrical arcing to the tissue. This apparatus was used as the sole method of thermal coagulation in 20 patients undergoing replacement of pacemaker batteries.

Diathermy↗

Carotid sinus syndrome: an overlooked cause of syncope.

Carotid sinus syncope was diagnosed during a 2-year period in 21 men and 5 women, aged 51 to 80 years, who had experienced 1 to 30 syncopal episodes during periods of time which varied from 1 day to 6 years. In 19 of these patients there was evidence of organic heart disease. Carotid sinus hypersensitivity of the cardioinhibitory type was present in 14 patients, the vasodepressor type in 1 patient, and a mixed type in 7 patients. In four patients with the cardioinhibitory response, the possibility of the vasodepressor response was not excluded. A pacemaker was placed in 17 patients, deferred in 4 patients and refused by 5 patients. Follow-up of patients with pacemakers over 9.5 +/- 7.0 (SD) months revealed recurrence of symptoms in two patients due to a previously unrecognized vasodepressor response. Follow-up of the patients without pacemakers was brief (4.6 +/- 3.7 months), and they remained asymptomatic, except for one patient with recurring vertigo.

Aged↗

Left and right ventricular function in inferior acute myocardial infarction and significance of advanced atrioventricular block.

Of 139 consecutive patients with a first inferior acute myocardial infarction, 26 (19%) had advanced atrioventricular (AV) block and 113 (81%) did not. All were evaluated by 2-dimensional echocardiography (2-D echo) and radionuclide angiography. Patients with advanced AV block had lower radionuclide left ventricular (LV) ejection fraction (51 +/- 10 vs 58 +/- 11%, p less than 0.01), higher LV wall motion score on 2-D echo (5.6 +/- 2.6 vs 3.1 +/- 2.7, p less than 0.001), lower radionuclide right ventricular (RV) ejection fraction (32 +/- 15 vs 39 +/- 16%, p less than 0.001) and higher RV wall motion score on 2-D echo (3.4 +/- 1.7 vs 1.5 +/- 2, p less than 0.002) than did patients without AV block. The incidence rate of RV dysfunction was higher in patients with advanced AV block (78 vs 40%, p less than 0.02), and the mortality rate was also higher (although not significantly) in patients with advanced AV block (15 vs 6%). In conclusion, patients with inferior acute myocardial infarction and advanced AV block have larger infarct sizes (as seen on radionuclide angiography and 2-D echo) and lower RV and LV function than patients without AV block. This finding may explain the higher mortality rate observed in this group.

Adult↗

Torsade de pointes due to quinidine: observations in 31 patients.

We performed a mail solicitation and obtained the records of 31 patients with documented torsade de pointes (TDP) due to quinidine. All 31 patients had heart disease: ischemic = 11 patients (36%), rheumatic = five patients (16%), hypertensive = four patients (13%), cardiomyopathic = four patients (13%), other = seven patients (22%). Quinidine was administered to these patients for the following reasons: atrial fibrillation or flutter = 22 patients (71%), ventricular premature beats = six patients (19%), ventricular or supraventricular tachycardia = three patients (10%). The 31 patients were receiving quinidine, 650 to 2400 (mean 1097) mg/day, and 14 patients had serum quinidine levels of 1.4 to 10.6 (mean 3.7) micrograms/ml. TDP occurred within 1 week of initiation of quinidine therapy in 23 (74%) of the patients. Twenty-eight (90%) of the 31 patients were receiving digoxin, and 5 (24%) of 21 patients had hypokalemia at the time of TDP. Off of quinidine therapy, corrected QT (QTc) intervals in 24 patients ranged from 390 to 580 (mean 470) msec and were prolonged in 17 patients (71%). On quinidine therapy, QTc intervals in 23 patients ranged from 390 to 630 (mean 510) msec and were prolonged in 21 patients (91%). In summary, patients with TDP due to quinidine usually had heart disease complicated by atrial fibrillation, were receiving digoxin, and were receiving moderate dosages of quinidine for less than 1 week prior to TDP. Approximately two thirds of patients with TDP due to quinidine had long QT intervals while off of quinidine.

Adolescent↗

Advanced early and late atrioventricular block in acute inferior wall myocardial infarction.

Seventy-six patients with acute inferior acute myocardial infarction (AMI) and advanced atrioventricular (AV) block are described. According to pre-established ECG criteria and time of appearance of the advanced AV block, patients were divided into two groups. The early block group consisted of 31 patients who developed advanced AV block during the hyperacute ECG stage of AMI. Advanced AV block in these patients was characterized by early appearance, short duration, third-degree type block, poor response to atropine, and increased need for pacemaker therapy. The late block group consisted of 45 patients who developed advanced AV block during subsequent ECG stages of AMI. Advanced AV block in these patients was characterized by late appearance, longer duration, second-degree type block, positive response to atropine, and diminished need for pacemaker therapy. Morbidity and mortality also differed between both groups. Patients with early block had more syncope (32% vs 2%, p less than 0.0001), more left heart failure (36 vs 7%, p less than 0.005), and more cardiogenic shock (39% vs 2%, p less than 0.001) than patients with late block. The mortality rate in the early block group was high (23%) and similar to that reported in the literature, whereas the mortality rate in the late block group was low (7%, p less than 0.05) and similar to the mortality rate reported for acute inferior AMI without advanced AV block. These data identify a subgroup of patients with acute inferior AMI and advanced AV block, which accounts for the high mortality rate reported in this group of patients.

Adult↗

Pharmacological observations in patients with nodoventricular pathways.

Three patients with accessory nodoventricular pathways and re-entry tachycardia are reported. In all three patients the accessory nodoventricular pathway formed the anterograde limb of the re-entry circuit while the His-Purkinje-atrioventricular node axis formed the retrograde limb of the tachycardia in two of the patients and a concealed accessory pathway formed the retrograde limb in the remaining patient. All three patients also manifested dual anterograde atrioventricular nodal pathways with conduction through the accessory nodoventricular pathways being associated with the atrioventricular nodal fast pathway. Type I antiarrhythmic drugs, especially disopyramide and quinidine, were effective for the treatment of the re-entry tachycardia because of their depressive action on the nodoventricular pathway. Beta blockers were also effective because of their action on the atrioventricular nodal portion of the re-entry circuit in one patient and most probably due to atypical (atrioventricular nodal like) properties of a retrogradely conducting accessory pathway in a second patient.

Adolescent↗

Right axis deviation in acute myocardial infarction. Clinical significance, hospital evolution, and long-term follow-up.

The incidence, in-hospital evolution, and long-term follow-up were studied in patients who developed acute deviation of the mean (frontal) QRS axis to the right during an acute myocardial infarction (AMI). Among 3,160 patients evaluated, 13 (0.41 percent) developed left posterior hemiblock (LPHB) and 57 (1.8 percent) developed an incomplete form of LPHB, the right axis deviation group (RAD). Patients in the LPHB group had a statistically significant higher incidence of in-hospital morbidity (69 percent incidence of congestive heart failure) and mortality (38.5 percent). Follow-up revealed a statistically significant higher incidence of cardiac symptomatology (angina pectoris and congestive heart failure) in the RAD group than in the control group, mainly in patients in whom RAD persisted for more than 24 hours. Patients developing LPHB during AMI constitute a high risk population with a high incidence of morbidity and mortality. Patients developing RAD constitute an intermediate group (between the LPHB and the control group) characterized by a high incidence of cardiac symptoms at the time of follow-up.

Angina Pectoris↗

Amiodarone-induced polymorphous ventricular tachycardia.

Five cases of amiodarone-induced polymorphous ventricular tachycardia (torsade de pointes) are presented. All patients had recurrent syncope or dizziness due to polymorphous ventricular tachycardia and in all cases the QT interval was prolonged. In two cases hypokalemia was present at the time the arrhythmia was first recorded, but in both cases polymorphous ventricular tachycardia persisted despite correction of the electrolyte imbalance. Standard treatment for polymorphous ventricular tachycardia (isoproterenol, ventricular pacing, or both) was successful in all patients, however, therapy had to be continued for 5 to 10 days, most probably because of the long elimination half-life of amiodarone.

Aged↗