Rodney W. Salo

Effect of Pacing Chamber and Atrioventricular Delay on Acute Systolic Function of Paced Patients With Congestive Heart Failure

BACKGROUND Previous studies of pacing therapy for dilated congestive heart failure (CHF) have not established the relative importance of pacing site, AV delay, and patient heterogeneity on outcome. These variables were compared by a novel technique that evaluated immediate changes in hemodynamic function during brief periods of atrial-synchronous ventricular pacing. METHODS AND RESULTS Twenty-seven CHF patients with severe left ventricular (LV) systolic dysfunction and LV conduction disorder were implanted with endocardial pacing leads in the right atrium and right ventricle (RV) and an epicardial lead on the LV and instrumented with micromanometer catheters in the LV, aorta, and RV. Patients in normal sinus rhythm were stimulated in the RV, LV, or both ventricles simultaneously (BV) at preselected AV delays in a repeating 5-paced/15-nonpaced beat sequence. Maximum LV pressure derivative (LV+dP/dt) and aortic pulse pressure (PP) changed immediately at pacing onset, increasing at a patient-specific optimal AV delay in 20 patients with wide surface QRS (180+/-22 ms) and decreasing at short AV delays in 5 patients with narrower QRS (128+/-12 ms) (P<0.0001). Overall, BV and LV pacing increased LV+dP/dt and PP more than RV pacing (P<0.01), whereas LV pacing increased LV+dP/dt more than BV pacing (P<0.01). CONCLUSIONS In this population, CHF patients with sufficiently wide surface QRS benefit from atrial-synchronous ventricular pacing, LV stimulation is required for maximum acute benefit, and the maximum benefit at any site occurs with a patient-specific AV delay.

Improvement of Cardiac Function in Patients with Severe Congestive Heart Failure and Coronary Artery Disease by Dual Chamber Pacing with Shortened AV Delay

Medical therapy often fails to control symptoms of severe heart failure. The possibility of modifying to some degree the global ventricular performance with the implantation of a physiological dual chamber pacemaker, set with a short atrioventricular delay (100 msec), has been adopted in two patients with severe heart failure due to coronary artery disease. The baseline clinical condition of both patients was characterized by leg edema, ascites, dyspnea at rest, or even orthopnea with a functional New York Heart Association (NYHA) class III‐IV. Acute measurements of hemodynamic and echocardiographic parameters during stepwise shortening of AV interval guided the pacemaker implantation and setting of AV delay in the chronic phase. Within a few days after pacemaker implantation, both patients considerably improved their clinical status as well as their functional NYHA class, improving to class U in one patient and to class II‐III in the other patient. In addition, modification of systolic and diastoJic parameters paralleled these improvements functional class and clinical condition. Pacemaker therapy in severe heart failure refractory to medical therapy can be of considerable benefit in patients whose quality‐of‐life is severely compromised when pharmacological therapy is no longer effective. Acute hemodynamic and echocardiographic testing is useful in assessing the most appropriate AV delay and pacing mode.

Acute hemodynamic improvement by pacing in patients with severe congestive heart failure.

Since the first report on dual chamber pacing for congestive heart failure (CHF) in 1991, a number of investigators have explored the topic with conflicting results. These conflicts may arise from an incomplete understanding of the mechanisms by which pacing improves cardiac function. Potential mechanisms include: (1) increase in filling time: (2) decrease in mitral regurgitation: (3) optimization of left heart mechanical atrioventricular delay (left heart MAVD); and (4) normalization of ventricular activation. One or more of these mechanisms may be operative in an individual patient, implying that patients may require individuol optimization. Acute pacing studies were conducted on nine CHF patients, NYHA Class II‐III to Class IV. Measurements of conduction times in sinus rhythm revealed: (1) normal interatrial conduction times (59 ± 5 ms) in all patients, with wide variations in interventricular conduction times (range, −15–105 ms); and (2) a wide range of left heart MAVD (range, 97–388 ms). While pacing the right, left, or both ventricles, measurement of high fidelity aortic pressure and mitral and aortic velocities revealed the following: (1) 6 of 9 patients increased mean pulse pressure over sinus value during RV orLV pacing at an optimal A V delay: (2) the maximum aortic pulse pressure was achieved when the atrium was not paced: an 8% increase over sinus pulse pressure with paced RV versus a 5% decrease for paced atrium and RV at optimum AV delay (paired Students t‐test, P = 0.01), and a 0% increase over sinus with paced LV versus 7% decrease for paced atrium and LV at optimum AV delay, P < 0.05: (3) significant dependence on pacing site was noted, with 4 patients doing best with RV pacing. 3 patients achieving a maximum with LV pacing, and 2 patients showing no preference; and (4) 2 of 4 patients with restrictive filling patterns were converted to nonrestrictive patterns with optimum pacing. Patient hemodynamics appear to benefit acutely from individually optimized pacing. Increases in filling time, optimization of left heart MAVD, and normalization of intraventricular activation are the most significant mechanisms. Atrial pacing is inferior to atrial sensed modes if the patient has a functional sinus node.

Measurement of Ventricular Volume by Intracardiac Impedance: Theoretical and Empinrcal Approaches

The most widely used equation, V = pL2/R, is developed for the computation of ventricular volume from catheter based impedance measurements. The assumptions implicit in this derivation are examined and found to be generally invalid. An empirical discrete resistor model is described which includes the impedance of the myocardial tissue and the adjoining ventricular blood volume. Once the parameters of this model are determined for individual canine hearts, the model predicts stroke volume from measured impedances. Due to the difficulty involved in determining the parameters of the empirical model, a numerical model is developed which solves the equation V ¿a V U + F = 0 in a three-dimensional volume. This model is then used to determine the effect of parallel tissue resistance, catheter position, and contraction of the other ventricle on volumes computed by intracardiac impedance. Parallel tissue resistance is found to have the greatest impact on absolute volume measurements. However, stroke volume computations are relatively unaffected by any of the three factors.

Rate responsive cardiac pacemaker

Pacemaker technology continues to advance in the direction of restoring a normal hemodynamic response under varying physiologic conditions. Rate-responsive pacemakers meet this challenge by adjusting the pacing rate in response to a sensed physiologic variable other than sinus node activity. In an effort to design the ideal rate-responsive system, various physiologic cues have been tested. To translate shifts in the sensed physiologic indicator into an appropriate pacing rate, specialized sensor systems also have been developed and include mechanical, chemical, thermal, and electrical sensors. Although each sensor system offers advantages and disadvantages, continued research and clinical experience will determine the future of this exciting new form of cardiac pacing.

Ventricular Preexcitation Modulates Strain and Attenuates Cardiac Remodeling in a Swine Model of Myocardial Infarction

Background— Myocardial infarction modifies the distribution of stress within the heart, increasing wall stress in ischemic and surrounding tissue, which often leads to adverse left ventricular remodeling. Electrical preexcitation pacing with appropriate timing of high-stress regions can reduce local strain and may attenuate global remodeling. Methods and Results— Myocardial infarction was induced in 24 swine to study the short-term (n=12) and long-term (n=12) effects of therapy. Sonomicrometry and hemodynamic measurements were used to show the mechanistic effects of preexcitation and to determine the optimal stimulation site and atrioventricular delay. Lagrangian strain was used to assess regional loading characteristics. Long-term study animals were randomized to 8 weeks of preexcitation (therapy) or no pacing (control). Echocardiograms were performed 2 days after myocardial infarction and repeated at 60 days, when tissue weights and apoptosis were assessed. Preexcitation reduced regional strain in the short term, with the best results achieved when the border region was paced at an atrioventricular delay of 50% of the intrinsic PR interval. In the long term, the changes in left ventricular internal diameter and left atrial size were decreased in therapy animals versus control animals (0.9±0.3 versus 1.5±0.5 cm, P=0.03, and 1.06±0.78 versus 2.32±0.88 cm, P<0.04, respectively). Heart weight was significantly lower in the therapy animals than in the control animals (319.8±20.8 versus 359.6±29.3 g, P=0.02). Although not significant, cardiomyocyte apoptosis trended lower in the therapy group. Conclusions— Preexcitation of the left ventricle after myocardial infarction reduced strain and stroke work in the infarct and border regions in the short term and attenuated adverse ventricular remodeling in the long term.

Experimental validation of pulse contour methods for estimating stroke volume at pacing onset

Stroke volume (SV) might be an important variable in assessing cardiac function of patients under pacing therapy. To assess the accuracy of estimating SV changes from aortic pressure during VDD pacing, we implanted electromagnetic flowmeters in the aortic root of five mongrel dogs. Three pacing sites, including right ventricle, left ventricle and both ventricles were selected and paced at 5 atrioventricular delays. Each pacing site/AV delay combination was repeated 5 times in a randomized order. The protocol alternated 5 paced beats and 15 intrinsic beats. Flow and aortic pressure data were recorded and analyzed. We evaluated five pulse contour equations relating pulse pressure (PP), ejection time (ET), diastolic time (DT) and aortic pressure area during systole over the end-diastolic pressure (Psa). A good correlation (r=0.84-0.89) was shown between percent change in SV and percent change in PP, PP*ET, Psa, Psa*ET and Psa*(1+ET/DT) over the preceding baseline. The average estimated percent change in SV also correlated with the average measured percent change in SV for each pacing site/AV delay combination. In conclusion, PP, PP*ET, Psa, Psa*ET and Psa*(1+ET/DT) may be clinically applicable for assessing SV at the start of VDD pacing and may effectively predict the effects of pacing sites and AV delays on SV.

The feasibility of utilizing the systolic pre-ejection interval as a determinant of pacing rate☆

Rate-modulated pacing modes adjust the stimulus rate by responding to sensed alterations in physiologic indexes of metabolic demand. This study was designed to determine whether right ventricular pre-ejection interval, measured in patients by a prototype pacemaker system capable of tracking intraventricular volume, changes predictably with exercise and, if so, whether it can be used in an algorithm to vary heart rate appropriately. This system utilizes intraventricular electrical impedance measurements of injected microampere currents to determine intracavitary volume changes. Five pacemaker-dependent patients underwent temporary insertion of a tripolar electrode connected to an external device that sensed cardiac signals, generated an impedance wave form and produced stimuli at rates dependent on pre-ejection interval. Pre-ejection interval did not change as a result of variations in pacing rate itself (347 +/- 41 ms at 70 beats/min versus 321 +/- 19 ms at 130 beats/min), but consistently decreased during graded exercise (by 23% from baseline). During rate-modulated pacing based on pre-ejection interval, heart rate significantly increased during exercise compared with ventricular demand pacing (by 46 +/- 6 versus 7 +/- 6 beats/min, respectively), and increased appropriately during burst exercise. Thus, the pre-ejection interval appears to be a specific, reliable physiologic determinant of pacing rate during exertion, which may be applicable in implantable rate-modulated pacemakers.

Effect on Ventricular Performance of Direct Current Electrical Shock for Catheter Ablation of the Atrioventricular Junction

In ten patients undergoing catheter ablation of the atrioventric‐ular junction (CAVJ) because of therapy refractoriness of supraventricular arrhythmias, the effect of repeated high energy direct current (DC) shock on left ventricular function has been investigated. End‐systolic pressure‐volume relation (ESPVR) and the positive first derivative of ventricular pressure (dP/ dt) have been used as indices of left ventricular systolic function, while the time constant of isovolumic pressure decay, the diastolic stiffness, and the negative dP/dt represented the diastolic function parameters, respectively. Each patient received at least two and no more than three DC shocks for successful CAVJ, with an energy of 360 joules. Significant acute reduction of both systolic and diastolic function was noted after each DC shock, with a slow partial recovery of both phases. The recovery process involved the systolic phase earlier and more completely than the diastolic one. The alterations observed could not be predicted from preablation values, but were significantly related to cumulative energy dose index for body weight. In conclusion, repeated high energy DC shocks acutely, but reversibly, impair left ventricular function; in addition, the ventricular function reduction is primarily related to the total ablation energy indexed for body weight.

The Effect of VVI Pacing and Resultant Atrioventricular Dyssynchrony on Segmental Volumes

Left and right ventricular volumes were monitored simultaneously in four anesthetized dogs by intracardiac impedance ventriculography during normal sinus rhythm, spontaneous ventricular rhythm, and VVI and VDD pacing. Cardiac output was found to increase with VVI pacing rate but remained somewhat lower than normal sinus or VDD values. The dissynchronous atrial contraction was found to distort the volume waveforms but had little effect on right ventricular volumes. Left atrial contraction had the greatest impact on left ventricular filling at near normal AV delays. Cardiac output during VDD pacing was found to be a maximum at 170 msec and decreased in three of four dogs at 220 msec. Examination of volume waveforms during “filling” indicates that the right ventricle is dominated by passive filling while the left ventricle demonstrates a large active or “fast” filling phase.