Michael D. Gammage

Selective Site Pacing: Defining and Reaching the Selected Site

Selective site right ventricular pacing has been suggested as an approach to reduce the incidence of ventricular dysfunction and hopefully influence the morbidity resulting from traditional right ventricular apical pacing. Pacing from the right ventricular apex allows a stable ventricular rate, and together with atrial pacing and sensing, helps maintain atrioventricular synchrony but does not allow physiological activation of the left ventricle. Traditional atrial pacing sites like the right atrial appendage may encourage atrial tachyarrhythmias, whereas lead placement in right atrial septal sites may reduce the frequency of symptomatic atrial tachyarrhythmia episodes, especially when combined with prevention algorithms. Researchers attempting to pace the heart from these selective sites have been hindered by the lack of uniform definitions of where these sites actually lie and the inadequacy of tools to consistently reach these locations and verify correct placement. This lack of definition consensus may have contributed to the apparent conflict of data, particularly in the right ventricle. There is an urgent need for a standardization of terms and identifying measures for selective pacing sites. (PACE 2004; 27[Pt. II]:883–886)

CLINICAL EXPERIENCE WITH THERA DR RATE-DROP RESPONSE PACING ALGORITHM IN CAROTID SINUS SYNDROME AND VASOVAGAL SYNCOPE

This study examined the effectiveness of cardiac pacing using the Thera DR rate‐drop response algorithm for prevention of recurrent symptoms in patients with carotid sinus syndrome (CSS) or vasovagal syncope. The algorithm comprises both diagnostic and treatment elements. The diagnostic element consists of a programmable “window” used to identify heart rate changes compatible with an evolving neurally mediated syncopal episode. The treatment arm consists of pacing at a selectable rate and for a programmable duration. Forty‐three patients (mean age 53 ± 20.4 years) with CSS alone (n = 8), CSS in conjunction with vasovagal syncope (n = 4), or vasovagal syncope alone (n = 31) were included. Thirty‐nine had recurrent syncope, while the remaining four reported multiple presyncopal events. Prior to pacing, 40 ± 152 syncopal episodes (range from 1 to approximately 1,000 syncopal events) over the preceding 56 ± 84.5 months. Postpacing follow‐up duration was 204 ± 172 days. Three patients have been lost to follow‐up and in one patient the algorithm was disabled. Among the remaining 39 individuals, 31 (80%) indicated absence or diminished frequency of symptoms, or less severe symptoms. Twenty‐three patients (23/29, or 59%) were asymptomatic with respect to syncope or presyncope. Sixteen patients had symptom recurrences. Of these, seven experienced syncope (7/39, or 18%) and 9 (29%) had presyncope: the majority of patients with recurrences (6/7 syncope and 7/9 presyncope) were individuals with a history of vasovagal syncope. Consequently, although symptoms were observed during postpacing follow‐up, they appeared to be of reduced frequency and severity. Thus, our findings suggest that a transient period of high rate pacing triggered by the Thera DR rate‐drop response algorithm was beneficial in a large proportion of highly symptomatic patients with CSS or vasovagal syncope.

Cardiovascular function and glucocorticoid replacement in patients with hypopituitarism.

OBJECTIVE Retrospective analysis suggests an increased mortality from cardiovascular disease in hypo‐pituitary adults; GH deficiency has been postulated to account for this. However, glucocorticoid replacement doses of 30 mg/day of hydrocortisone (HC) may be excessive, and could therefore be implicated in the increased cardiovascular mortality in this group of patients. The aims of this study were to establish whether patients with hypopituitarism have any abnormalities of the cardiovascular system compared to a control group and whether any of these parameters might be improved by reducing the replacement dose of glucocorticoid.

Hyperthyroidism and Cardiovascular Morbidity and Mortality

Hyperthyroidism is a common disorder affecting multiple systems in the body. The cardiovascular effects are among the most striking. The availability of effective treatments for hyperthyroidism has led to the widespread perception that it is a reversible disorder without any long-term consequences. Recent evidence suggests, however, that there may be adverse outcomes. Long-term follow-up studies have revealed increased mortality from cardiovascular and cerebrovascular disease in those with a past history of overt hyperthyroidism treated with radioiodine, as well as those with subclinical hyperthyroidism. Thyroid hormones are known to exert direct effects on the myocardium, as well as the systemic vasculature and predispose to dysrhythmias, especially supraventricular. Atrial fibrillation (AF) is a recognized complication of overt hyperthyroidism, and subclinical hyperthyroidism is also known to be a risk factor for development of AF. Supraventricular dysrhythmias, particularly atrial fibrillation, in older patients may account for some of the excess cardiovascular and cerebrovascular mortality described, especially because AF is known to predispose to embolic phenomena.

Benefit of Single Setting Rate Responsive Ventricular Pacing Compared with Fixed Rate Demand Pacing in Elderly Patients

In order to assess the value of a simple, single setting rate response option to VVI pacing, 12 patients (mean age 75.1 ± 6,2, range 62–83 years, seven males, five females) with symptomatic complete heart block were entered into a double‐blind, randomized crossover trial of VVI versus VVIR (single setting rate responsive) pacing using Medtronic Activitrax pacemakers. Assessment was by time taken in seconds (sec) and Borg scale symptom score (6–20) for simple activities (standing from chair x 30; walking 800 meters; 52 steps on stairs [slow and fast pace], and incremental, noninclined maximal treadmill exercise), performed after a 4‐week period with the patient in each pacing mode. Times were significantly improved in VVIR mode for standing from chair [mean ± SD] (78.7 ± 22.5 vs 70.7 ± 19.5 sec; P < 0.05), for 800 m walk (1032 ± 80 vs 885 ± 59 sec; P < 0.05), fast ascent of stairs (29.5 ± 7.7 vs 26.5 ± 5.6 sec; P < 0.02), and treadmill exercise (626.7 ± 189.5 vs 741.0 ± 170.2 sec, P < 0.005) although no difference in time for slow stair ascent was demonstrated. Symptom scores were significantly less in VVIR for standing from chair (12.7 ± 2.8 vs 10.3 ± 1.8; P < 0.01), 800 m walk (10.9 ± 2.7 vs 9.0 ± 2.4; P < 0.01), slow ascent of stairs (11.6 ± 2.1 vs 10.0 ± 2.0; P < 0.01), and fast ascent of stairs (13.0 ± 2.0 vs 11.7 ± 1.9; P < 0.02) but unchanged for treadmill exercise. Single setting VVIR pacing increases maximum exercise capacity and decreases perceived difficulty of submaximal exercise in elderly patients with symptomatic heart block. This would be a beneficial addition to most limited and multiprogrammable VVI systems for use in the elderly.

Thyroid disease and its treatment: short-term and long-term cardiovascular consequences

Thyroid hormones exert important effects on the cardiovascular system, including effects on cardiac systolic and diastolic function, peripheral vascular resistance and arrhythmogenesis. Hyperthyroidism and hypothyroidism often cause opposing effects on cardiovascular physiology in the short term. Increasing evidence suggests that long-term vascular morbidity and mortality occurs in both overt and subclinical thyroid disease.

Rate-Drop Response Cardiac Pacing for Vasovagal Syncope

Recent reports suggest that cardiac pacing incorporating a rate-drop response algorithm is associated with a reduction in the frequency of syncopal episodes in patients with apparent cardioinhibitory vasovagal syncope. The detection portion of the algorithm employs a programmable heart rate change-time duration “window” to both identify abrupt cardiac slowing suggestive of an imminent vasovagal event and trigger “high rate” pacing. The purpose of this study was to develop recommendations for programming the rate-drop response algorithm. Pacemaker programming, symptom status, and drug therapy were assessed retrospectively in 24 patients with recurrent vasovagal syncope of sufficient severity to warrant consideration of pacemaker treatment. In the 53±19 months prior to pacing, patients had experienced an approximate syncope burden of 1.2 events/month. During follow-up of 192±160 days, syncope recurred in 4 patients (approximate syncope burden, 0.3 events / month, p < 0.05 vs. pre-pacing), and pre-syncope in 5 patients. In these patients, rate-drop response parameters were initially set based on electrocardiographic and/or tilt-table recordings, and were re-programmed at least once in 14 (58%) individuals. A 20 beat/min window height (top rate minus bottom rate), a window width of 10 beats (61% of patients), and 2 or 3 confirmation beats (79% of patients) appeared to be appropriate in most patients. Treatment intervention rate was set to >100 beats/min 89% of patients, with a duration of 1 to 2 min in 79%. In conclusion, a narrow range of rate-drop response parameter settings appeared to be effective for most individuals in this group of highly symptomatic patients.

A Synopsis: Neurocardiogenic Syncope, An International Symposium, 1996

Neurally mediated or neurocardiogenic syncopai syndromes,^ especially vasovagal syncope and carotid sinus syndrome (CSS), amount for the largest proportion of faints encountered in clinical practice. Nonetheless, despite such prominence, our understanding of the pathophysiological hasis for these forms of syncope remains limited,̂ * and the optimal strategies for diagnosis and treatment of these conditions continue to be a source of dehate. This international symposium, the proceedings of which are reflected in this PACE supplement, brought together engineers, physicians, and physiologists recognized for their interest in and ongoing contributions to the understanding of neurally mediated (neurocardiogenic) syncope and its management. The principal goals were to address current understanding of those aspects of circulatory control that contribute to neurally mediated faints, review the current status of diagnostic and treatment strategies, and provide direction for the next investigational steps. A particular focus of interest was the potential for implantable devices to play a role in the management of neurally mediated syncope in the most severely affected patients. As is often the case in symposia of this type, many valuable contributions and insights occurred unexpectedly during poster presentations and discussion periods. Thanks to the efforts of several diligent note-takers, many of these ideas and criticisms were documented. In this synopsis. we attempt to summarize certain key elements of the symposium, incorporating where possible additional spontaneous comments provided by members of the expert audience.

Permanent Pacemaker Positioning Via the Inferior Vena Cava in a Case of Single Ventricle with Loss of Right Atrial-Vena Cava Continuity

Successful dual chamber pacing was achieved by implanting permanent pacemaker leads using an extra‐peritoneal approach to the inferior vena cava in a 48‐year‐old patient with a single ventricle, transposition of the great vessels, and a right atrial pulmonary artery shunt (Glenns procedure). The pacemaker generator was implanted into a subcutaneous pockel in the anterior abdominal wall.

Effect of experimental hypertension on phosphoinositide hydrolysis and proto-oncogene expression in cardiovascular tissues.

Products of inositol lipid hydrolysis and levels of c-myc, c-fos and H-ras mRNAs were measured in rat left ventricle and vascular tissues 72 h and 9 days after the induction of aortic coarctation in order to examine inositol phosphate and proto-oncogene signals during the development of pressure-related cardiac and vascular structural changes. There was a significant increase in left ventricular and proximal aortic mass at both time points but no change in mesenteric resistance artery morphology in rats with coarctation. At 72 h there was a significant increase in c-myc, c-fos and H-ras mRNAs in the left ventricle of rats with coarctation, and this was accompanied by increased levels of inositol (1,4,5)-trisphosphate. Similar results were obtained in the proximal but not the distal aorta. In resistance arteries inositol phosphate production and proto-oncogene mRNA expression were unchanged. The results indicate that at 72 h aortic coarctation induced structural thickening in the left ventricle and proximal aorta and was associated with increased inositol phosphate production and stimulation of specific proto-oncogene mRNAs. By 9 days following surgery much of the structural change in these tissues was completed, and these raised cellular signals were no longer observed. The results suggest that both increased inositol lipid hydrolysis and a rise in the expression of these proto-oncogenes are important processes in the development of vascular hypertrophy seen in this model of hypertension.