Kara J. Quan

Mechanisms of Heart Rate and Arterial Blood Pressure Control: Implications for the Pathophysiology of Neurocardiogenic Syncope

Neurocardiogenic syncope is a general term that describes syncope resulting from altered autonomic activity, as manifested by abnormal regulation of peripheral vascular resistance and heart rate. Although there has been great interest in the contribution of heart rate to this form of syncope, the peripheral circulation plays the dominant role in the induction of neurocardiogenic syncope in most patients. We review in this brief article the physiology of cardiovascular reflexes, which are important for short‐term arterial pressure control, and their potential contribution to the pathophysiology of neurocardiogenic syncope. This type of syncope represents a profound failure of the normal mechanisms for short‐term regulation of arterial pressure. Any therapeutic strategies for the management of neurocardiogenic syncope must deal with alterations in vascular control, which contribute to its pathogenesis.

Characterization of sinoatrial parasympathetic innervation in humans.

Sinoatrial Parasympathetic Innervation. Introduction: The response to sinoatrial parasympathetic nerve stimulation (shortened atrial refractoriness) was used to determine the atrial distribution of these nerve fibers in humans. We hypothesized that, in humans, parasympathetic nerves that innervate the sinoatrial node also innervate the right atrium and that the greatest density of innervation is near the sinoatrial nodal fat pad.

Intracardiac alternans compared to surface T-wave alternans as a predictor of ventricular arrhythmias in humans

BACKGROUND Microvolt T-wave alternans (MTWA) measured from the surface electrocardiogram (ECG) is a marker of sudden cardiac death (SCD). Recently, it has been suggested that intracardiac alternans (ICA) detected from the endocardium underlies MTWA and is a marker of electrical instability leading to ventricular arrhythmias. As such, ICA may be used in future implantable cardioverter-defibrillators (ICDs) to monitor periods of electrical instability before ICD therapy. We examined whether electrical instability, as measured by MTWA, can be detected by ICA located from the right ventricle and if ICA can predict ventricular arrhythmias in patients with ICDs. METHODS Both MTWA and ICA were measured simultaneously during atrial pacing in 68 patients undergoing electrophysiology study (EPS). ICA was measured from unipolar electrograms acquired from a catheter at the apical, mid, and basal regions of the right ventricle in 48 patients and at the apical region alone in 20 patients. Indications for EPS included nonsustained ventricular tachycardia, cardiomyopathy, syncope, near syncope, or palpitation. RESULTS Fifty-six of 68 patients had cardiomyopathy with left ventricular ejection fraction (LVEF) <or= 0.40. Mean LVEF was 0.29 +/- 0.13. ICA was detected at either the apex or base in 11 patients. ICA was concordant with MTWA in 87% (59 of 68) of the patients. ICA occurred at a greater magnitude than MTWA (3 +/- 2 mV vs. 2 +/- 2 microV, P <0.05). At a mean follow up of 4 years, 50% (34 of 68) of patients had an ICD implanted. Of patients with either a positive ICA or MTWA test, 49% (8 of 17) had an ICD implanted with appropriate shock in 75% (6 of 8) of the patients. Of patients with both normal ICA and MTWA tests, 51% (26 of 51) had an ICD for primary prevention, and appropriate ICD therapies occurred in 27% (7 of 26). After 1 year follow-up in patients with ICDs, the positive predictive values of ICA and MTWA in predicting ventricular arrhythmias were 14% and 17%, respectively. The negative predictive values for ICA and MTWA were both 82% at 4 years. CONCLUSION ICA is detectable from the right ventricle and can predict the patients at low risk for ventricular arrhythmias. Future applications of ICA may provide an integral part of arrhythmia detection and development of algorithms to divert shock therapy in ICDs.

Endocardial stimulation of efferent parasympathetic nerves to the atrioventricular node in humans: Optimal stimulation sites and the effects of digoxin

AbstractThe purposes of this study were to identify optimal sites of stimulation of efferent parasympathetic nerve fibers to the human atrioventricular node via an endocardial catheter and to investigate the interaction between digoxin and vagal activation at the end organ. Methods: The ventricular rate was measured during atrial fibrillation, prior to and during parasympathetic nerve stimulation, in 8 patients taking digoxin and in 10 controls. High frequency electrical stimuli were delivered via an hexapolar or quadripolar electrode catheter, placed at the posteroseptal right atrium near the atrioventricular node (n=18 patients) or in the coronary sinus (n=12 of 18 patients). In 4 patients, stimulation was repeated after intravenous administration of 1 to 2[emsp4 ]mg of atropine. Results: Nerve stimulation prolonged the R-R interval in all patients. Stimulation close to the posteroseptal right atrium led to maximal atrioventricular nodal slowing. The mean R-R intervals at baseline and during parasympathetic nerve stimulation (60[emsp4 ]mA) from the posteroseptal right atrium and the proximal coronary sinus were 581±79[emsp4 ]ms, 2440±466, and 900±228[emsp4 ]ms respectively (p=0.0001). The response to nerve stimulation was greater in patients taking digoxin than in patients not taking the drug (p=0.02). Junctional rhythm occurred during nerve stimulation in 8/8 patients taking digoxin and 0/10 not taking the drug (p=0.0001). The response to stimulation was eliminated after atropine (p=0.01). Conclusions: Parasympathetic nerves to the atrioventricular node were stimulated from the proximal coronary sinus as well as the posteroseptal right atrium. Stimulation at the posteroseptal right atrium resulted in the greatest response, and digoxin enhanced this response. The augmented response suggests that an interaction may exist between parasympathetic stimulation and digoxin at the end organ.

Favorable results of implantable cardioverter-defibrillator implantation in patients older than 70 years

BACKGROUND The clinical results of implantable cardioverter-defibrillator (ICD) implantation in the elderly have received limited documentation. As the longevity of the U.S. population has increased, so has the need for ICD implantation in the elderly. We evaluated the efficacy and outcome of ICD implantation in elderly patients (>70 years) compared with younger patients. METHODS The case records of all consecutive patients who underwent ICD implantation at our institution between 1986 and 1994 were reviewed. Of a total of 238 patients, 78 patients were 70 years of age or older and 160 patients were younger than 70 years of age. RESULTS The mean age of the younger group was 58 years and that of the elderly group was 74 years. There were no statistical differences in the presence of coronary artery disease, left ventricular systolic function, the inducibility of arrhythmias, or the history of sudden cardiac death. The hospital morbidity rate was similar in both groups (6.9% in the younger group and 7.7% in the elderly group; p = not significant). The operative mortality rate was 1.9% for the younger group and 1.3% for the elderly group (p = not significant). At a mean follow-up of 33 +/- 26 months, Kaplan-Meier survival curves demonstrated similar survival rates, with 93%, 82%, and 65% of the patients alive at 1, 3, and 6 years, respectively. CONCLUSIONS Implantable cardioverter-defibrillator implantation was equally effective in the treatment of patients older than 70 years as in younger patients. No differences in theoretic survival or morbidity were observed.

Type I primary hyperoxaluria: an unusual presentation of ventricular tachycardia.

A 42-year-old woman sought treatment for palpitation, chest heaviness, and dyspnea. A rhythm strip from the emergency squad documented a wide complex tachycardia (Fig. 1). Past medical history included end-stage renal disease requiring hemodialysis, nephrolithiasis, and a failed living-related donor renal transplant. On physical examination, multiple skin ulcers were noted. A diffuse laterally displaced point of maximal impulse, normal heart sounds, and a II/VI systolic murmur over the left precordium were documented. Echocardiography revealed biventricular dysfunction, mitral regurgitation, and tricuspid regurgitation. The ejection fraction was 0.20, and the pulmonary artery pressure was 60 mmHg. Amiodarone was initiated for the ventricular tachycardia. Cardiac catheterization revealed normal coronary arteries. Dermatologic and kidney biopsies were performed (Figs. 2 and 3). The differential diagnosis included amyloidosis, sarcoidosis, primary oxalosis, systemic lupus erythematosus, and Lyme disease. Dermatologic and kidney biopsies confirmed calcium oxalate crystals. Primary oxalosis is a rare hereditary disorder of metabolism resulting in accumulation of calcium oxalate in tissues. A deficiency of the liver enzyme alanine glyoxylate aminotransferase is present. Glyoxylate is converted to oxalate, which combines with calcium, causing calcium oxalate nephrolithiasis. The clinical manifestations are mostly renal; however, calcium oxalate can accumulate in all tissues, including the heart. Right bundle branch block, dilated cardiomyopathy, complete heart block, and ventricular arrhythmias have been described. In the literature, 4 patients with cardiac manifestations have undergone combined liver and kidney transplantation. In our patient, the diagnosis of type I primary hyperoxaluria was confirmed by dermatologic and kidney biopsies, and she underwent successful liver and kidney transplantation. Several weeks posttransplant, an electrophysiologic study was performed. Monomorphic ventricular tachycardia was induced despite amiodarone therapy. An implantable cardioverter-defibrillator was placed. An echocardiogram obtained approximately 60 months after liver and kidney transplantation revealed an ejection fraction of

Implantable cardioverter defibrillator (ICD) for polymorphic ventricular tachycardia (VT) due to coronary vasospasm

We report a case of a young woman who presented with atypical angina. During an episode of chest pain she had a documented run of sustained polymorphic ventricular tachycardia (VT). In addition to medical therapy, she received an ICD to prevent future episodes of sudden cardiac death.

Cardiac Pacemakers – Past, Present, and Future

Publisher Summary This chapter presents a brief history of cardiac pacemakers and discusses the features of present day pacemakers. The first pacemaker devices could only externally stimulate the heart. Output voltage and stimulation rates were controlled from the front panel of the pacemaker. The electrodes were two one-inch diameter metal discs placed on the right and left sides of the chest, held in place by a rubber strap. Infection was a frequently fatal complication of these devices, and after transistors became available, the implantation of smaller fully implantable pacemaker units became possible. The first implantable device had a diameter of 55 mm and thickness of 19 mm, had two stainless steel electrodes sutured to the epicardium, and was externally rechargeable every month. The main developments during the early years were lead technology, capsule housing, and mainly battery life. The transvenous route for placing electrodes became available in 1959 and with the introduction of central vein catheterization access, non surgeons cardiologists also started to implant pacemakers. Early pacers were asynchronous with the patients own rhythm, and were only capable of delivering an electrical stimulus to the heart at a steady rate. The next challenge in pacemaker technology was to attempt to restore atrioventricular synchrony. A bifocal pacemaker was introduced, which could pace the atria, and after an appropriate AV interval would pace the ventricle. Complications from pacemakers can be divided into the long-term effects or risks of chronic pacing as well as device-, lead-, or implantation-related complications. Device-related complications mainly include hardware failure and tissue injury from stress, infection, or allergic reactions. Pacemaker related infections may involve cardiac tissue, leads, and the cutaneous and subcutaneous tissue and their treatment options include antibiotic therapy, removal of the implanted system, and tissue debridement.

Spontaneous Inversion of an Implanted Defibrillator

A 67‐year‐old man with ischemic cardiomyopathy received an implantable defibrillator for ventricular fibrillation 3 years ago. He now presents with weight loss and an inability to interrogate or establish any telemetric communication with his defibrillator. An abdominal radiograph was obtained (right) that, when compared to a film obtained 5 months earlier (left) illustrated a significant change in the position of the device. Inspection of the manufacturer radiographic