Mode of Onset of Malignant Ventricular Arrhythmias in Idiopathic Ventricular Fibrillation

Mode of Onset of Idiopathic VF. Introduction : The mode of onset of malignant ventricular arrhythmias (ventricular tachycardia [VT] or ventricular fibrillation [VF] has been well described in patients with organic heart disease and in patients with the long QT syndromes. Less is known about the mode of onset of VF in patients with out-of-hospital VF who have no evidence of organic heart disease or identifiable etiology.
Methods and Results : We reviewed the ECGs of all our patients with Idiopathic VF. Documentation of the onset of spontaneous arrhythmias was available for 22 VK episodes in 9 patients (6 men and 3 women; age 41 ± 16 years). In all instances, spontaneous VF followed a rapid polymorphic VT, which was initiated by premature ventricular complexes (PVCs) with very short coupling intervals. The PVC initiating VF had a coupling interval of 302 ± 52 msec and a prematurity index of 0.4 ± 0.07. These PVCs occurred within 40 msec of the peak of the preceding T wave. Pause-dependent arrhythmias were never observed.
Concltision : Cardiac arrest among patients with idiopathic VF has a very distinctive mode of onset. Documentation of a polymorphic VT that is not pause dependent is of diagnostic value.     

Right Bundle Branch Block of Unknown Age in the Setting of Acute Anterior Myocardial Infarction: An Attempt to Define Who Should Be Paced Prophylactically

It is widely accepted that patients presenting with acute anterior myocardial infarction and acute onset of right bundle branch block should be prophylactically paced in contrast with those who have a chronic bundle branch block. The admitting physician is faced with the dilemma of how to act if the age of this conduction disturbance is unknown. This problem has further intensified in recent years, with the introduction of thrombolytic treatment, where insertion of a central vascular line is associated with increased morbidity. The objectives of this study were to define clinical or electrocardiographic parameters that may help the admitting physician to decide whether patients presenting with an anterior wall myocardial infarction and a right bundle branch block of unknown age should be prophylactically paced. We examined prospectively the in-hospital clinical course of 39 consecutive patients presenting with an acute myocardial infarction in whom the age of a right bundle branch block upon admission was unknown (group C, n = 39) and compared it with two similar groups of patients who presented with an acute right bundle branch block (group A, n = 38) and with a known chronic right bundle branch block (group B, n = 22). Thirty-three patients (33%) died, with cardiogenic shock being the leading cause of death in the entire population. Prophylactic pacing, which was carried out in 66% and 54% of patients in groups A and C, respectively, did not reduce mortality rates. No clinical or electrocardiographic variables on admission were predictive to support prophylactic pacing in group C. In 10 of 46 (22%) patients who were prophylactically paced with a transvenous electrode, the following complications attributed to the procedure were detected: (1) either rapid sustained ventricular tachycardia (during implantation) that was unresponsive to overdrive pacing, or ventricular fibrillation necessitating electrical defibrillation (4 patients); (2) recurrent episodes of rapid nonsustained ventricular tachycardia, which stopped only after the pacemaker was turned off (1 patient); (3) complete AV block (1 patient); (4) fever appearing on the third or fourth day after implantation (3 patients); and (4) a large hematoma in the groin in 1 patient who was treated with thrombolysis shortly before pacemaker electrode insertion. Thus, the complications of transvenous temporary pacing in the era of thrombolysis may outweigh any theoretical advantage. (PACE 1995; 18:1496-1508)     

Change in very low-, low-, and high-density lipoproteins during lipid lowering (bezafibrate) therapy: studies in type IIA and type IIb hyperlipoproteinaemia

The effects of lipid lowering therapy (bezafibrate) on plasma lipoproteins was investigated in twelve patients with familial hypercholesterolaemia (type IIA) and eight with familial combined hyperlipidaemia (type IIB). Bezafibrate caused a decrease of plasma cholesterol, plasma triglycerides, plasma apolipoprotein B, VLDL cholesterol and LDL cholesterol and an increase of HDL cholesterol. Post-heparin plasma lipoprotein and hepatic lipase activities increased in both groups (significant only in type IIB). Lipoprotein composition showed the following changes: Increased protein and phospholipids and decreased triglycerides and cholesteryl esters in VLDL. Decreased protein and triglycerides and increased free and esterified cholesterol in LDL. Decreased triglycerides and increased phospholipids in HDL. Cholesteryl ester to protein ratios decreased in VLDL and increased in LDL. The hydrated density of LDL (both groups) and of HDL3 (type IIB) decreased following bezafibrate therapy. These changes were in general similar to those observed in hypertriglyceridaemic patients and could be ascribed, at least in part, to the increase of plasma lipase activities and the decrease of lipid transfer reactions. Comparing the present data with that previously reported, it was found that bezafibrate caused decreased LDL cholesterol in types IIA and IIB but increased levels in type IV. This change was correlated with the initial plasma triglycerides (r = 0.74, P less than 0.0001) and initial plasma LDL cholesterol (r = 0.66, P less than 0.001). It is concluded that varied response of LDL to therapy reflects a complex interaction of metabolic events, including changing rates of VLDL conversion to LDL, lipoprotein compositional changes and effects of therapy on LDL degradation rates.     

Recurrent Laryngeal Nerve Paralysis Following Pacemaker Introduction

Electrode insertion to the heart via subclavian vein puncture has become a commonplace procedure. A case is presented in which employment of this route led to permanent paralysis of the recurrent laryngeal nerve. (PACE, Vol. 5, July-August, 1982)     

FIXED AND DYNAMIC URETHRAL COMPRESSION FOR THE TREATMENT OF POST-PROSTATECTOMY URINARY INCONTINENCE: IS HISTORY REPEATING ITSELF?

PURPOSE: We reviewed the evolution of appliances and devices used for treating post-prostatectomy urinary incontinence. MATERIALS AND METHODS: We used the MEDLINE to search the literature from 1966 to March 2000 and then manually searched bibliographies to identify studies that our initial search may have missed. RESULTS: The evolution of treatment for post-prostatectomy urinary incontinence may be traced back to the 18th century. Two main schools of thoughts simultaneously evolved. The first fixed urethral compression devices were constructed to enable urethral obstruction by fixed resistance. This outlet resistance allows voiding after intra-abdominal and intravesical pressure is elevated but it is sufficient to prevent leakage between urinations. The other school of thought preferred creation of dynamic urethral compression in which outlet resistance is not fixed but may be decreased when voiding is desired or elevated between urinations. Therapeutic fixed and dynamic urethral compression interventions may be further divided into external or internal compressive devices or procedures. External fixed compression devices may be traced back to antiquity. A penile clamp, similar to the later Cunningham clamp, and a truss designed to compress the urethra by external perineal compression were presented in the Heister textbook of surgery, Institutiones Chirurgicae, as early as 1750. Dynamic compressive devices applied externally were developed much later, such as the first artificial urinary sphincter, described by Foley, in 1947 and the Vincent apparatus, described in 1960. The modern era of fixed urethral compression began in 1961 with Berry. Acrylic prostheses impregnated with bismuth to allow radiographic visualization were produced in various shapes and sizes, and used to compress the urethra against the urogenital diaphragm. In 1968 the University of California-Los Angeles group under the direction of Kaufman began to use cavernous crural crossover to compress the bulbous urethra (Kaufman I). Later 2 other modifications were described, including approximation of the crura in the midline using a polytetrafluoroethylene mesh tape (Kaufman II) and an implantable silicone gel prosthesis (Kaufman III). With the advent of the artificial urinary sphincter pioneered by Scott in 1973 interest in passive urethral compression disappeared in favor of the implantation of an inflatable circumferential prosthetic sphincter. Recently there has been a trend back to passive urethral compression. Synthetic bolsters have been described that passively compress the bulbar urethra to achieve urinary incontinence after radical prostatectomy. CONCLUSIONS: Much creativity has been dedicated to solve the complex and challenging problem of post-prostatectomy urinary incontinence. Devices used for treating this condition may be grouped according to the mechanism of action and how they are applied. Passive urethral compression, long abandoned in favor of dynamic implantable sphincters, has reemerged. Further research in this field may determine which school of thought may provide the best solution for treating post-prostatectomy urinary incontinence.     

The Effect of Metal Detector Gates on Implanted Permanent Pacemakers

The effect of metal detector security gates, such as are used in airports, was tested in 103 nonselected pacemaker patients. Various types of single and dual chamber units were examined, using telemetry during the test. Pulse rate and duration were measured immediately before and after the procedure. No ill effect was seen on any of the units tested, pacemaker inhibition was not observed, and programmability was not affected. Metal detector security gates have no effect on implanted permanent pacemakers.     

Effect of magnesium on restenosis after percutaneous transluminal coronary angioplasty: a clinical and angiographic evaluation in a randomized patient population: A pilot study

Restenosis is a major clinical problem following successfulpercutaneous transluminal coronary angioplasty. Since magnesiumhas vasodilator and antithrombotic effects, this study was designedto evaluate its potential to decrease the rate of restenosis. In an open-labelled, randomized controlled study, 148 patientsunderwent successful coronary angioplasty. Ninety-eight patientswere treated with 46—52 mmoll 18–20 h intravenousmagnesium sulphate (groups Ml and M2), and 49 of them continuedwith oral supplements of magnesium hydroxide 600 mg. day^–1(group M2).The other 50 patients served as controls (group C).Coronary angiography was performed before, immediately afterand at 6 months follow-up or earlier if clinically indicated.Clinical, laboratory, ergometric and radionuclide evaluationswere also carried out. One hundred and thirty-nine patients (94%) with 163 dilatedsegments completed the study. Intravenous magnesium was welltolerated The cross-sectional area at the site of angioplastyincreased by 3.55 ± 201 mm2 in groups Ml and M2 comparedwith an increase of 2.90 ± 163 mm2 in the control group,(P=003). A trend towards a lower rate of restenosis (>50%reduction in luminal diameter) was noticed in the magnesiumgroups (28/110, 25%) compared with the control group (20/53,38%) P=0.10. Oral administration of magnesium was well tolerated,did not have an additive effect on restenosis, but an improvedclinical course was noted. It is concluded that intravenous administration of magnesiumin patients undergoing coronary angioplasty is feasible andsafe and that the beneficial trend of magnesium to prevent acuterecoil and late (within 6 months) restenosis is encouragingand should promote further investigation in a larger patientpopulation.