The increasing prevalence of congestive heart failure has focused importance on the search for potentially reversible etiologies of cardiomyopathy. The concept that incessant or chronic tachycardias can lead to ventricular dysfunction that is reversible is supported by both animal models of chronic rapid pacing as well as human studies documenting improvement in ventricular function with tachycardia rate or rhythm control. Sustained rapid pacing in experimental animal models can produce severe biventricular systolic dysfunction. Hemodynamic changes occur as soon as 24 h after rapid pacing, with continued deterioration in ventricular function for up to 3 to 5 weeks, resulting in end-stage heart failure. The recovery from pacing-induced cardiomyopathy demonstrates that the myopathic process associated with rapid heart rates is largely reversible. Within 48 h after termination of pacing, hemodynamic variables approach control levels, and left ventricular ejection fraction shows significant recovery with subsequent normalization after 1 to 2 weeks. In humans, descriptions of reversal of cardiomyopathy with rate or rhythm control of incessant or chronic tachycardias have been reported with atrial tachycardias, accessory pathway reciprocating tachycardias, atrioventricular (AV) node reentry and atrial fibrillation (AF) with rapid ventricular responses. Control of AF rapid ventricular responses has been demonstrated to improve ventricular dysfunction with cardioversion to sinus rhythm, pharmacologic ventricular rate control and AV junction ablation and permanent ventricular pacing. The investigation of potential tachycardia-induced cardiomyopathy in patients with heart failure requires further prospective confirmation in larger numbers of patients, with study of mechanisms, patient groups affected and optimal therapies.

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Although rate responsive pacing based on impedance minute ventilation (IMV) is now standard, there is almost no data confirming the relationship between IMV from an implanted pacemaker and measured minute ventilation (VE) during exercise. Nineteen completely paced adults implanted with Medtronic Kappa 400 pacemakers underwent symptom-limited maximal metabolic treadmill testing using a modified Minnesota Pacemaker Response Protocol. Minute ventilation (VE, L/min) was simultaneously measured using the flowmeter of a respiratory metabolic gas analysis system and the transthoracic impedance minute ventilation circuitry of the pacemaker. Correlation coefficients (r) were used to find the best fit line to describe the relationship between the two measurements. Mean (+/- SD) r values for the first, second, and third order polynomial equations and for log and exponential equations were: 0.92 +/- 0.08, 0.94 +/- 0.04, 0.95 +/- 0.04, 0.91 +/- 0.06, and 0.91 +/- 0.07, respectively. None of the r values were statistically different from the first order equation. Transthoracic IMV as measured by the Medtronic Kappa 400 is closely correlated to measured minute ventilation and is represented well by a first order (linear) equation.

DURU, F., ET AL.: Influence of Posture, Breathing Pattern, and Type of Exercise on Minute Ventilation Es timation by a Pacemaker Transthoracic Impedance Sensor. Previous studies have shown a high correla tion between transthoracic impedance minute ventilation (IMV) determined by a pacemaker sensor and actual minute ventilation (VÉ) measured by standard methods. We hypothesized that several factors (e.g., posture, breathing pattern, and exercise type) could potentially affect the calibration between IMV and V¿. In patients with Medtronic Kappa 400 pacemakers, V¿ (L/min) was monitored using a standard cardiopulmonary metabolic gas analysis system with simultaneous recording of IMV (ohms/min) using DR-180 extended telemetry monitors. Effects of posture and of breathing pattern at rest (19 patients; age 60 ± 13 years) were evaluated by monitoring each patient under three conditions: (a) slow breathing, supine, (b) slow breathing, sitting, and (c) shallow breathing, supine. Calibration at rest was defined as the ratio of IMV to V¿. Effect of type of exercise on calibration compared treadmill versus graded bicycle ergometer exercise (18 patients; age 62 ± 14 years). Calibration during exercise was defined as: (a) "Begin" (the IMV to VÉ ratio at VÉ =10 L/min, the typical VÉ value at beginning of exercise), and (b) slope of the IMV/VÈ regression line. Calibration of IMV/VÉ was significantly smaller for sitting versus supine position (0.7130.177, P < 0.001) and for shallow versus slow breathing (0.7210.373, P< 0.001), and larger for tread mill versus bicycle exercise (Begin: 1.240.43, P = 0.018; Slope: 1.260.42, P = 0.013). In conclusion, pos ture, breathing pattern, and type of exercise affect the IMV estimation of the actual VÉ, possibly by alter ing the static or dynamic geometry (thus, the impedance) of the intrathoracic viscera. (PACE 2000; 23[Pt.II]:1767-1771 pacemaker, rate response, sensors, impedance, minute ventilation

Previous studies showed that transthoracic impedance minute ventilation (IMV), as measured by a pacemaker sensor, is closely correlated to actual minute ventilation (VE) determined by standard methods. The aim of this study was to analyze the changes in the calibration between IMV and VE at rest and during exercise over time. Fifteen patients (age 60 +/- 13 years) with Medtronic Kappa 400 pacemakers completed a baseline visit followed by two visits separated by 1 month and 1 week, respectively. In each patient, VE (L/min) was monitored at rest in the supine and sitting positions and during graded bicycle ergometer exercise using a standard cardiopulmonary metabolic gas analysis system with simultaneous recording of IMV (omega/min) using DR-180 extended telemetry monitors. Calibration at rest was defined as the ratio of IMV to VE, calculated from 1-minute average values in the supine and sitting positions. Calibration during bicycle exercise was defined as intercept (IMV value at VE = 10 L/min-typical VE value at beginning of exercise), and slope of the IMV/VE regression line. The calibration of IMV showed individual variability over time. The magnitude (absolute value) of observed fractional changes in calibration at 1 month was 0.23 +/- 0.20 (rest-supine), 0.20 +/- 0.15 (rest-sitting), 0.18 +/- 0.19 (exercise-intercept), 0.28 +/- 0.35 (exercise-slope), and 0.18 +/- 0.15, 0.15 +/- 0.09, 0.28 +/- 0.39, and 0.27 +/- 0.15, respectively, at 1 week. The magnitude of change at 1 month was not statistically different from the magnitude of change at 1 week. In conclusion, the calibration of IMV, as measured by a pacemaker sensor, versus actual VE may demonstrate variability. However, this study also suggests that the observed changes are not cumulative over time. These results have implications for patient monitoring applications using these sensors and for development of future pacemaker rate response algorithms.

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