Juan M. Juanteguy
Johns Hopkins University
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Juan M. Juanteguy.
Pacing and Clinical Electrophysiology | 1984
M. Mirowski; Philip R. Reid; Morton M. Mower; Levi Watkins; Edward V. Platia; Lawrence S.C. Griffith; Juan M. Juanteguy
The automatic implantable cardioverter‐defibrillator is an electronic device designed to monitor the heart continuously, to identify malignant ventricular tachyarrhythmias, and then to deliver effective countershock to restore normal rhythm. There are two defibrillating electrodes which are also used for waveform analysis; one is located in the superior vena cava, the other is placed over the cardiac apex. A third bipolar right ventricular electrode serves for rate counting and R‐wave synchronization. When ventricular fibrillation occurs, a 25 joule pulse is delivered; when ventricular tachycardia faster than a preset rate is detected, the discharge is R‐wave synchronized. The device can recycle three times if required. Special batteries can deliver over 100 shocks or provide a 3‐year monitoring life. Implantation of the device is made either through a thoracotomy or by a subxiphoid approach. Thus far, the device has been implanted in 160 patients with a follow‐up of 42 months. Acceleration of ventricular tachycardia to a faster rhythm or to ventricular fibrillation occurred only rarely and is dealt with most successfully through recycling. Actuarial analysis of the initial 52 patients has indicated 22.9% one‐year total mortality, a 52% decrease from the 48% mortality that would be expected in the same group of patients without the device: the mortality attributed to arrhythmias was only 8.5%. In conclusion, the automatic cardioverter‐defibrillator can reliably identify and correct potentially lethal ventricular tachyarrhythmias, leading to a substantial increase in survival in properly selected high‐risk patients.
Journal of the American College of Cardiology | 1987
Igor Singer; Grover M. Hutchins; M. Mirowski; Morton M. Mower; Enrico P. Veltri; Thomas Guarnieri; Juan M. Juanteguy; Sara Fisher; Philip R. Reid; Myron L. Weisfeldt
The purpose of the present study was to examine at autopsy the effect of multiple defibrillations on the myocardium and the pathologic consequences of short- and long-term placement of the intravascular and interpericardial leads of the automatic implantable cardioverter-defibrillator. Twenty-five patients were examined at autopsy; 8 of them underwent lead implantation only and 17 received both leads and the automatic implantable cardioverter-defibrillator. Twelve patients (48%) died of ventricular tachycardia or ventricular fibrillation; seven (28%) died of other causes. Acute pericarditis occurred in all patients, resulting in a localized, progressive fibrosis around the apical patch lead without giving rise to pericardial restriction. Thrombus formation was associated with the superior vena cava spring electrode in four patients (17%) and the right ventricular rate-sensing electrode in one patient (4%). Asymptomatic pulmonary emboli occurred in two patients (8%). In one patient who underwent defibrillation 59 times, superior vena cava changes consisted of vein wall destruction, fibrosis and thrombus formation. Pathologic changes under the apical patch related to defibrillation were observed in seven patients; two of these had fewer than 5 defibrillations, one had 8 defibrillations and four had 21 to 74 defibrillations. These changes consisted of contraction band necrosis in four patients, vacuolar cytoplasmic clearing and loss of myocytes confined to the myocardium under the patch electrode in five patients who had multiple defibrillations. The observed pathologic changes were estimated to affect less than 2% of the total myocardial mass. Thus, the automatic implantable cardioverter-defibrillator lead system and multiple defibrillations result in localized myocardial injury confined to the tissue under the patch electrode.(ABSTRACT TRUNCATED AT 250 WORDS)
Pacing and Clinical Electrophysiology | 1991
Terrance Khastgir; J. John Lattuca; Diana Aarons; Joseph Murphy; Vicki O'mara; Juan M. Juanteguy; Enrico P. Veltri
To assess the effect of defibrillation and amiodarone on ventricular pacing threshold and time to capture in patients undergoing automatic implantable cardioverter‐defibrillator (AICD) implantation, 28 patients were prospectively evaluated. The patients were entered into one of two protocols: la—epicardial ventricular pacing threshold measured at baseline (preventricular fibrillation induction) and 10 and 60 seconds postdefibrillation with 20 J, or Ib—two fibrillation‐defibrillation sequences were performed 3 minutes apart and ventricular pacing thresholds were measured for each sequence at baseline and at 10 and 60 seconds postdefibrillation with 20 J. Ten patients also underwent asynchronous pacing at 1.1 times baseline threshold during ventricular fibrillation with measurement of time to capture postdefibrillation. All patients were randomly assigned to receive either amiodarone or no antiarrhythmic drug therapy. Ventricular fibrillation was induced with AC (applied for 1‐2 seconds), and standard epicardial bipolar and epicardial patch electrodes of the AICD were used for pacing and defibrillation, respectively. Ventricular pacing threshold at baseline, 10 seconds, 60 seconds, and 3 minutes postdefibrillation did not differ significantly. There were no significant differences in patients with or without amiodarone therapy. Furthermore, there was no transient loss of ventricular capture postdefibrillation or significant difference in time to capture with amiodarone (≤ 2 seconds). We conclude that following internal defibrillation with 20 J: (1) ventricular pacing threshold at 10 seconds, 60 seconds, and 3 minutes were not significantly different from baseline with one or two fibrillation‐defibrillation sequences, (2) time to capture was short, and (3) there was no significant difference in no drug versus amiodarone. These findings have direct clinical importance in considering device therapy with both pacing and defibrillating capabilities.
Journal of Cardiac Surgery | 1988
Levi Watkins; Thomas Guarnieri; Lawrence S.C. Griffith; Joseph Levine; Enrico P. Veltri; Juan M. Juanteguy; Morton M. Mower; M. Mirowski
Since February 1980 the automatic implantable cardioverter defibrillator has been implanted in over 1,500 patients. Sudden death rates have been reduced to 2%–4% annually. This report reviews the implantation techniques, their indications, and our clinical experience in 200 patients.
Archive | 1987
M. Mirowski; Morton M. Mower; Enrico P. Veltri; Juan M. Juanteguy
Because the treatment of ventricular fibrillation and many hemodynamically unstable ventricular tachycardias with electrical countershock is critically dependent on rapid availability of medical personnel and equipment, its implementation outside the hospital is rarely successful. This situation has prompted the development of a fully implantable automatic device designed for continuous monitoring of the heart rhythm and prompt recognition and treatment of life-threatening ventricular tachyarrhythmias [1]. Since the first implantation of such a device in a human being at The Johns Hopkins Hospital [1], the automatic implantable cardioverter-defibrillator (AICD*) is being used with increased frequency to prevent sudden cardiac death in high-risk patients [2–8]. The growing clinical experience has demonstrated that this therapeutic intervention dramatically lowers the prohibitive arrhythmic mortality of this population [3, 8, 9].
Annals of the New York Academy of Sciences | 1984
M. Mirowski; Philip R. Reid; Morton M. Mower; Levi Watkins; Edward V. Platia; Lawrence S.C. Griffith; Juan M. Juanteguy
Although the pathogenesis of life-threatening ventricular arrhythmias is now better understood, their prevention and treatment remain a formidable task. In spite of increased public awareness of the problem and introduction into clinical practice of new drugs and surgical techniques, out-of-hospital arrhythmic death continues to claim great numbers of victims. The difficulties inherent in dealing with malignant ventricular arrhythmias when they occur in the community reflect the fact that their only effective treatment consists of immediate application of an electrical countershock to the heart. Up to now, prompt availability of medical personnel and the presence of specialized equipment were absolutely indispensable for implementation of the life-saving maneuver. Whereas cardiopulmonary resuscitation lengthens the time available for effective defibrillation, and mobile emergency services shorten the time that elapses from onset of arrhythmia to initiation of treatment, the total dependence of these approaches on the involvement of trained personnel have restricted their life-saving potential to only a small fraction of the stricken patients. It is against this background that the concept of the automatic implantable defibrillator has been put f0rward.lAfter years of developmental research, the first animal implant occurred in 1976,3 and the initial human trial began in 1980.4 At the present time, the number of patients who have undergone implantation of the automatic defibrillator is about 150, and a broader clinical application of this new therapeutic modality appears to be imminent. The automatic implantable cardioverterdefibrillator can best be defined as an electronic device designed to continuously monitor the electrical activity of the heart, identify malignant ventricular rhythms, and then deliver effective countershock to restore normal heart action. The main purpose of this selfcontained diagnostic-therapeutic system is to prevent sudden death in selected high-risk patients whenever and wherever they are stricken by a malignant arrhythmia. Because the device performs its functions promptly and automatically, the constraints of time and the need for trained personnel, the two major stumbling blocks in conventional pre-hospital resuscitation, are largely eliminated.
Pacing and Clinical Electrophysiology | 1984
M. Mirowski; Philip R. Reid; Morton M. Mower; Levi Watkins; Edward V. Platia; Lawrence S.C. Griffith; Thomas Guarnieri; Andra Thomas; Juan M. Juanteguy
Pacing and Clinical Electrophysiology | 1984
Philip R. Reid; Lawrence S.C. Griffith; Morton M. Mower; Edward V. Platia; Levi Watkins; Juan M. Juanteguy; M. Mirowski
Pacing and Clinical Electrophysiology | 1984
Morton M. Mower; Philip R. Reid; Levi Watkins; Lawrence S.C. Griffith; Edward V. Platia; Stanley M. Bach; Mir Imran; Juan M. Juanteguy; M. Mirowski
JAMA Internal Medicine | 1992
Todd J. Cohen; Philip R. Reid; Morton M. Mower; M. Mirowski; Diana Aarons; Juan M. Juanteguy; Enrico P. Veltri