Left ventricular pacing minimizes diastolic ventricular interaction, allowing improved preload-dependent systolic performance.

BACKGROUND: Left ventricular (LV) pacing improves hemodynamics in patients with heart failure. We hypothesized that at least part of this benefit occurs by minimization of external constraint to LV filling from ventricular interaction. METHODS AND RESULTS: We present median values (interquartile ranges) for 13 heart failure patients with LV pacing systems implanted for New York Heart Association class III/IV limitation. We used the conductance catheter method to measure LV pressure and volume simultaneously. External constraint was measured from the end-diastolic pressure-volume relation recorded during inferior vena caval occlusion, during LV pacing, and while pacing was suspended. External constraint to LV filling was reduced by 3.0 (4.6 to 0.6) mm Hg from 4.8 (0.6 to 7.5) mm Hg (P<0.01) in response to LV pacing; effective filling pressure (LV end-diastolic pressure minus external constraint) increased by 4.0 (2.2 to 5.8) mm Hg from 17.7 (13.3 to 22.6; P<0.01). LV end-diastolic volume increased by 10 (3 to 11) mL from 238 (169 to 295) mL (P=0.01), whereas LV end-systolic volume did not change significantly (-1 [-2 to 3] mL from 180 [124 to 236] mL, P=0.97), which resulted in an increase in stroke volume of 11 (5 to 13) mL from 49 (38 to 59) mL (P<0.01). LV stroke work increased by 720 (550 to 1180) mL . mm Hg from 3400 (2110 to 4480) mL . mm Hg (P=0.01), and maximum dP/dt increased by 120 (2 to 161) mm Hg/s from 635 (521 to 767) mm Hg/s (P=0.03). CONCLUSIONS: This study suggests a potentially important mechanism by which LV pacing may produce hemodynamic benefit. LV pacing minimizes external constraint to LV filling, resulting in an increase in effective filling pressure; the consequent increase in LV end-diastolic volume increases stroke volume via the Starling mechanism.

Left ventricular pacing improves haemodynamic variables in patients with heart failure with a normal QRS duration.

OBJECTIVES: To assess whether patients with congestive heart failure (CHF) and a normal QRS duration can benefit from left ventricular (VDD-LV) pacing. DESIGN: Cardiac resynchronisation is reserved for patients with a broad QRS duration on the premise that systolic resynchronisation is the mechanism of benefit, yet improvement from pacing correlates poorly with QRS duration. In CHF patients with a broad QRS duration, those with a high resting pulmonary capillary wedge pressure (PCWP) > 15 mm Hg benefit. In this acute haemodynamic VDD-LV pacing study, patients with CHF with a normal QRS duration were divided into two groups--patients with a resting PCWP > 15 mm Hg and patients with a resting PCWP < 15 mm Hg--to determine whether benefit is predicted by a high resting PCWP. PATIENTS: 20 patients with CHF, New York Heart Association functional class IIb-IV, all with a normal QRS duration (< or = 120 ms). INTERVENTIONS: Temporary pacing wires were positioned to enable VDD-LV pacing and a pulmonary artery catheter was inserted for measurement of PCWP, right atrial pressure, and cardiac output. RESULTS: In patients with a PCWP > 15 mm Hg (n = 10), cardiac output increased from 3.9 (1.5) to 4.5 (1.65) l/min (p < 0.01), despite a fall in PCWP from 24.7 (7.1) to 21.0 (6.2) mm Hg (p < 0.001). In patients with a PCWP < 15 mm Hg there was no change in PCWP or cardiac output. Combined data showed that PCWP decreased from 17.0 (9.1) to 15.3 (7.7) mm Hg during VDD-LV pacing (p < 0.014) and cardiac output increased non-significantly from 4.7 (1.5) to 4.9 (1.5) (p = 0.125). CONCLUSIONS: Patients with CHF with a normal QRS duration and PCWP > 15 mm Hg derive acute haemodynamic benefit from VDD-LV pacing.

Ventricular interaction and external constraint account for decreased stroke work during volume loading in CHF.

The slope of the stroke work (SW)-pulmonary capillary wedge pressure (PCWP) relation may be negative in congestive heart failure (CHF), implying decreased contractility based on the premise that PCWP is simply related to left ventricular (LV) end-diastolic volume. We hypothesized that the negative slope is explained by decreased transmural LV end-diastolic pressure (LVEDP), despite the increased LVEDP, and that contractility remains unchanged. Rapid pacing produced CHF in six dogs. Hemodynamic and dimension changes were then measured under anesthesia during volume manipulation. Volume loading increased pericardial pressure and LVEDP but decreased transmural LVEDP and SW. Right ventricular diameter increased and septum-to-LV free wall diameter decreased. Although the slopes of the SW-LVEDP relations were negative, the SW-transmural LVEDP relations remained positive, indicating unchanged contractility. Similarly, the SW-segment length relations suggested unchanged contractility. Pressure surrounding the LV must be subtracted from LVEDP to calculate transmural LVEDP accurately. When this was done in this model, the apparent decrease in contractility was no longer evident. Despite the increased LVEDP during volume loading, transmural LVEDP and therefore SW decreased and contractility remained unchanged.

Acute effects of vitamin C on platelet responsiveness to nitric oxide donors and endothelial function in patients with chronic heart failure.

Chronic heart failure (CHF) is characterized by a prothrombotic state, which may relate to increased platelet aggregability, endothelial dysfunction, and increased oxidative stress. We investigated the effect of vitamin C in CHF on ex vivo platelet aggregation and platelet responsiveness to the anti-aggregatory effects of the nitric oxide (NO) donors glyceryl trinitrate (GTN) and sodium nitroprusside (SNP). We also examined parameters of oxidative stress and endothelial function in patients. In this double-blind, randomized, crossover study vitamin C (2 g) or placebo was given intravenously to 10 patients with CHF. We measured adenosine 5-diphosphate (ADP)-induced platelet aggregation, flow-mediated dilatation (FMD) in the brachial artery using ultrasonic wall-tracking, and plasma levels of lipid-derived free radicals using electron paramagnetic resonance spectroscopy. Vitamin C did not affect ex vivo platelet aggregability but enhanced the inhibition of platelet aggregation by SNP (62.7+/-10.2 to 82.7+/-4.8%, p = 0.03) and tended to increase responses to GTN (40.5+/-9.0 to 53.4+/-7.3, p = 0.06). The effect of vitamin C on platelet responsiveness to the antiaggregatory effects of SNP was inversely related to basal response to SNP (r = -0.9, p < 0.01); a similar trend was observed with GTN (r = -0.6, p = 0.1). Vitamin C also increased FMD (1.9+/-0.6 to 5.8+/-1.5%, p = 0.02) and reduced plasma lipid-derived free radicals by 49+/-19% (p < 0.05). In patients with CHF acute intravenous administration of vitamin C enhances platelet responsiveness to the anti-aggregatory effects of NO donors and improves endothelial function, suggesting a potential role for vitamin C as a therapeutic agent in CHF.

Preservation of venous endothelial function in the forearm venous capacitance bed of patients with chronic heart failure despite arterial endothelial dysfunction.

OBJECTIVES: The goal of this study was to assess whether endothelial dysfunction occurs in the forearm venous capacitance bed of patients with chronic heart failure (CHF) and to determine the role of nitric oxide (NO) in modulating venous tone. BACKGROUND: Control of venous tone is crucially important in CHF. More than 70% of blood volume lies in the venous capacitance beds. Therefore, small changes in venous tone may markedly affect cardiac filling pressures and cardiac output. METHODS: Venous tone was measured using radionuclide forearm venous plethysmography in 24 patients with CHF and 16 age-matched controls. The effect of basal NO activity on venous tone was assessed by infusing N-monomethyl-L-arginine 12 mg/min and stimulated NO using carbachol 15 microg/min. Brachial artery flow-mediated dilation was assessed by ultrasonic wall-tracking. RESULTS: Blockade of basal NO release caused a significant and similar venoconstriction in patients (9.6 +/- 1.8%, p < 0.01) and controls (6.6 +/- 1.7%, p < 0.01). Carbachol-induced venodilation was significant and similar in patients (36.8 +/- 3.9%, p < 0.001) and controls (40.7 +/- 3.9%, p < 0.001). Brachial artery flow-mediated dilation was impaired in patients compared with controls (2.0 +/- 0.6% vs. 7.5 +/- 2.5%, p < 0.01). CONCLUSIONS: Our data indicate that, despite marked impairment of the function of the arterial endothelium, there is preservation of both basal and stimulated NO release in the forearm venous capacitance bed. This may provide important insights into mechanisms of endothelial dysfunction in CHF and the potential for novel therapy.

Evidence against oxidative stress as mechanism of endothelial dysfunction in methionine loading model.

Endothelial dysfunction reflects reduced nitric oxide (NO) bioavailability due to either reduced production, inactivation of NO, or reduced smooth muscle responsiveness. Oral methionine loading causes acute endothelial dysfunction in healthy subjects and provides a model in which to study mechanisms. Endothelial function was assessed using flow-mediated dilatation (FMD) of the brachial artery in humans. Three markers of oxidative stress were measured ex vivo in venous blood. NO responsiveness was assessed in vascular smooth muscle and platelets. Oral methionine loading induced endothelial dysfunction (FMD decreased from 2.8 +/- 0.8 to 0.3 +/- 0.3% with methionine and from 2.8 +/- 0.8 to 1.3 +/- 0.3% with placebo; P < 0.05). No significant changes in measures of plasma oxidative stress or in vascular or platelet sensitivity to submaximal doses of NO donors were detected. These data suggest that oxidative stress is not the mechanism of endothelial dysfunction after oral methionine loading. Furthermore, the preservation of vascular and platelet NO sensitivity makes a signal transduction abnormality unlikely.

Neutrophil superoxide anion--generating capacity, endothelial function and oxidative stress in chronic heart failure: effects of short- and long-term vitamin C therapy.

OBJECTIVES: First, we sought to study the effects of short- and long-term vitamin C therapy on oxidative stress and endothelial dysfunction in chronic heart failure (CHF), and second, we sought to investigate the role of neutrophils as a cause of oxidative stress in CHF. BACKGROUND: Oxidative stress may contribute to endothelial dysfunction in CHF. Vitamin C ameliorates endothelial dysfunction in CHF, presumably by reducing oxidative stress, but this is unproven. METHODS: We studied 55 patients with CHF (ischemic and nonischemic etiologies) and 15 control subjects. Flow-mediated dilation (FMD) in the brachial artery was measured by ultrasound wall-tracking, neutrophil superoxide anion (O2-) generation by lucigenin-enhanced chemiluminescence and oxidative stress by measurement of free radicals (FRs) in venous blood using electron paramagnetic resonance (EPR) spectroscopy and plasma thiobarbituric acid reactive substances (TBARS). Measurements were performed at baseline in all subjects. The effects of short-term (intravenous) and long-term (oral) vitamin C therapy versus placebo were tested in patients with nonischemic CHF. RESULTS: At baseline, FRs were higher in patients with CHF than in control subjects (p < 0.01), TBARS were greater (p < 0.005), neutrophil O2- -generating capacity was enhanced (p < 0.005) and FMD was lower (p < 0.0001). Compared with placebo, short-term vitamin C therapy reduced FR levels (p < 0.05), tended to reduce TBARS and increased FMD (p < 0.05), but did not affect neutrophil O2- -generating capacity. Long-term vitamin C therapy reduced FR levels (p < 0.05), reduced TBARS (p < 0.05) and improved FMD (p < 0.05), but also reduced neutrophil O2- -generating capacity (p < 0.05). Endothelial dysfunction was not related to oxidative stress, and improvements in FMD with vitamin C therapy did not relate to reductions in oxidative stress. CONCLUSIONS: Oxidative stress is increased in ischemic and nonischemic CHF, and neutrophils may be an important cause. Vitamin C reduces oxidative stress, increases FMD and, when given long term, decreases neutrophil O2- generation, but the lack of a correlation between changes in endothelial function and oxidative stress with vitamin C implies possible additional non-antioxidant benefits of vitamin C.

Endothelium-derived nitric oxide contributes to the regulation of venous tone in humans.

BACKGROUND: Although nitric oxide (NO) is known to play an important part in the regulation of arterial tone, little is known about its role in veins. The aim of this study was to investigate the role of basal and stimulated NO activity in the regulation of tone of the human venous capacitance bed. METHODS AND RESULTS: We measured venous tone using radionuclide forearm venous plethysmography in 24 healthy subjects with no cardiovascular risk factors. In 13 subjects, basal NO activity was assessed by measuring the effects on venous tone of an intra-arterial infusion of the NO synthase inhibitor N-monomethyl-L-arginine (L-NMMA). In the remaining 11 subjects, stimulated NO activity was evaluated by measuring the effects of an intra-arterial infusion of incremental doses of carbachol, followed in a subgroup by coinfusion with L-NMMA. Infusion of carbachol caused dose-dependent venodilation, with a maximal reduction in forearm venous tone of 40.1+/-12.5% (P<0.0001). Carbachol-induced venodilation was inhibited by L-NMMA (48.9+/-6.2% reversal of maximal venodilation, P<0.01). Infusion of L-NMMA alone caused venoconstriction (9.1+/-6.4% increase in venous tone, P=0.002). CONCLUSIONS: Human forearm capacitance veins exhibit both stimulated and basal NO activity, which indicates that NO contributes not only to the regulation of venous tone but also to resting venous tone in healthy human subjects.

Pacing in heart failure: improved ventricular interaction in diastole rather than systolic re-synchronization.

AIMS: To determine the mechanism by which left ventricular and biventricular pacing works. BACKGROUND: Pacing for congestive heart failure patients is employed in those with left bundle branch block on the basis that it will improve discoordinated contraction; however, the response is unpredictable. The authors propose that the mechanism of benefit is rather related to improvement of ventricular interaction in diastole (VID). VID is found in patients with a high left ventricular end-diastolic pressure (> 15 mmHg). Left ventricular pacing in these patients will delay right ventricular filling and allow greater left ventricular filling before the onset of VID. METHODS: The study group consisted of 18 congestive heart failure patients with an ejection fraction < 30% and with no more than Grade 1 mitral regurgitation. Group I comprised 10 patients with pulmonary capillary wedge pressure > 15 mmHg, four patients had a normal QRS duration and six had left bundle branch block. Group II comprised eight patients with pulmonary capillary wedge pressure < 15 mmHg, of whom five had a normal QRS duration. Haemodynamics were measured at baseline and during VDD pacing from either the left ventricle or right ventricle. RESULTS: The ratio of stroke volume/pulmonary capillary wedge pressure was calculated as an index of the relationship between left ventricular end-diastolic pressure and contractile function. This ratio was lower in group I than in group II patients (P = 0.005). In group I, haemodynamics were improved with left ventricular pacing (stroke volume/pulmonary capillary wedge pressure increased from 2.2 +/- 0.9 to 4.4 +/- 3.6, P = 0.03). In group II there was no response to either left ventricular or right ventricular pacing. The improvement with left ventricular pacing was unrelated to QRS duration (r = 0.09). CONCLUSIONS: Left ventricular pacing acutely benefits congestive heart failure patients with pulmonary capillary wedge pressure > 15 mmHg irrespective of left bundle branch block. The present data suggest that the mechanism of response may be an improvement in left ventricular filling rather than ventricular systolic re-synchronization.

Diastolic ventricular interaction and ventricular diastolic filling.

Because the ventricles share a common septum, the filling of one may influence the compliance of the other, a phenomenon known as direct diastolic ventricular interaction (DVI). This interaction is markedly enhanced when the force exerted by the surrounding pericardium is raised (pericardial constraint). In health, in the resting state, we operate near the top of the flat component of a J-shaped pericardial stress-strain relation. Therefore, pericardial constraint (and hence DVI) is only minor. When right ventricular volume/pressure acutely increases, such as during exercise, massive pulmonary embolism, or right ventricular infarction, pericardial constraint increases and significant DVI develops. In this setting, the measured left ventricular intracavitary diastolic pressure markedly overestimates the true left ventricular filling pressure, because the external forces must be subtracted. Although the pericardium can grow during chronic cardiac enlargement, we present evidence that in certain chronic disease processes, including heart failure, DVI may also be important.

Reflex responses of venous capacitance vessels in patients with hypertrophic cardiomyopathy.

1. The aim of this study was to determine if there is impaired reflex venoconstriction in patients with hypertrophic cardiomyopathy and whether this is related to a history of syncope or exercise hypotension. 2. Thirty percent of patients with hypertrophic cardiomyopathy have exercise-induced hypotension associated with a failure of arteriolar constriction. Impaired venoconstriction could exacerbate this situation. 3. We evaluated 43 patients with hypertrophic cardiomyopathy and 24 controls. Nuclear venous plethysmography was used to measure forearm venous capacitance during lower body negative pressure, splenic venous volume changes during bicycle exercise and blood pressure responses to treadmill exercise. We assessed any association between abnormal reflex venous control and a history of syncope and exercise hypotension. 4. The percentage reduction in unstressed forearm venous volume during lower body negative pressure was similar in patients and controls (8.9 +/- 7.1% versus 9.7 +/- 5.9%, P not significant). Patients with a history of syncope demonstrated a less marked percentage reduction in volume than those without (-2.1 +/- 6.9% versus -10.6 +/- 6.0%, P = 0.001). In three patients with a history of syncope there was a paradoxical increase in forearm venous volume during lower body negative pressure. During exercise there was a substantially smaller decrease in splenic venous volume in patients compared with controls (-20.1 +/- 14.0% and -42.6 +/- 12.6% respectively, P = 0.0001). Furthermore, there was an association between attenuated splenic venoconstriction or venodilation and exercise hypotension in patients (P = 0.005). 5. Abnormal reflex control of venous capacitance beds in patients with hypertrophic cardiomyopathy was associated with both syncope and exercise hypotension.

Reduced cardiopulmonary baroreflex sensitivity in patients with hypertrophic cardiomyopathy.

OBJECTIVES: We sought to assess baroreflex function in patients with hypertrophic cardiomyopathy (HCM). BACKGROUND: We have previously demonstrated a specific abnormality in the afferent limb of the cardiopulmonary baroreflex in patients with vasovagal syncope. Patients with HCM exhibit abnormal control of their vasculature during exercise and upright tilt; we therefore hypothesize a similar abnormality in the afferent limb of the cardiopulmonary baroreflex arc. METHODS: We investigated 29 patients with HCM and 32 control subjects. Integrated baroreceptor sensitivity was assessed after administration of phenylephrine. Cardiopulmonary baroreceptor sensitivity was assessed by measuring forearm vascular resistance (FVR) during lower body negative pressure (LBNP). Carotid artery baroreflex sensitivity was assessed by measuring the in RR interval during manipulation of carotid artery transmural pressure. The integrity of the efferent limb of the reflex arc was determined by studying responses to both handgrip and peripheral alpha-receptor sensitivity. RESULTS: During LBNP, FVR increased by only 2.36+/-9 U in patients, compared with an increase of 123+/-8.76 U in control subjects (p=0.001). FVR paradoxically fell in eight patients, but in none of the control subjects. Furthermore, FVR fell by 4.9+/-5.6 U in patients with a history of syncope, compared with an increase of 4.7+/-7.2 U in those without syncope (p=0.014). Integrated and carotid artery baroreflex sensitivities were similar in patients and control subjects (14+/-7 vs. 14+/-6 ms/mm Hg, p=NS and -3+/-2 vs. -4+/-2 ms/mm Hg, p=NS, respectively). Similarly, handgrip responses and the dose/response ratio to phenylephrine were not significantly different. CONCLUSIONS: This study suggests that patients with HCM have a defect in the afferent limb of the cardiopulmonary reflex arc.

Forearm vascular responses during semierect dynamic leg exercise in patients following myocardial infarction.

We assessed forearm vascular and blood pressure responses to dynamic leg exercise in patients 7 and 28 days postmyocardial infarction. To determine a possible association between abnormal exercise vascular responses and baroreflex dysfunction, integrated and carotid baroreflex sensitivity and forearm vascular responses (during application of subhypotensive lower body negative pressure) were assessed. On day 7, 42 patients were compared with 21 age- and sex-matched controls. All subjects were assessed for (1) forearm vascular resistance during semierect exercise, (2) blood pressure measurements during erect treadmill exercise, and (3) integrated, cardiopulmonary, and carotid baroreceptor sensitivity. These studies were repeated in 13 patients on day 28. Forearm vascular resistance increased during exercise by 36% +/- 63% in patients versus 121% +/- 105% in controls (P = 0.0001), and fell in 15 patients, a response seen in none of the controls. Exercise hypotension was demonstrated in 5 patients, all of whom had abnormal vasodilator vascular responses. Those patients with vasodilator responses had a lower left ventricular ejection fraction (52% +/- 12% vs 62% +/- 9%; P = 0.007), and lower cardiopulmonary mechanoreceptor sensitivity (-6.6 +/- 3.9 units vs +6.4 +/- 10.4 units, P = 0.02) than those with constrictor responses, respectively. In the 13 patients studied on day 28, the change in forearm vascular resistance was similar to that observed on day 7 (36% +/- 63% vs 46% +/- 73%). Paradoxical vasodilation of forearm vessels during leg exercise is common in patients studied 7 and 28 days postmyocardial infarction, and is associated with lower left ventricular ejection fraction and abnormal vascular responses during subhypotensive lower body negative pressure.

A rate responsive pacemaker that physiologically reduces pacing rates at rest.

Current rate responsive pacemakers incorporate sensors such as minute ventilation (MV) for adapting to changing patient conditions during exercise and periods of exertion. However, for sleep and/or rest periods, the only pacemakers currently on the market that slow the pacing rate utilize an internal timer to determine a decrease in pacing rate. It would be advantageous if the pacing rate could be automatically lowered during periods of sleep or rest. This study utilized a rate responsive sensor, MV, to track the patient's sleeping and resting periods and to decrease the pacing rate at such times. A total of eight patients implanted with Sentri 1210 single chamber MV sensor pacemakers were studied. A sleep rate (SR) of 45 beats/min was selected. A sleep rate response function, which indicated the relationship between changes in MV and corresponding heart rate, was initially set at a value of 16 and continually and automatically updated in a 3-month study. Adaptation was based on the premise that 3 hours per day should be spent at the SR. The average decrease in pacing rates from onset to 3 month for the eight patients was 12.4% +/- 5.3%. Correspondingly, the histograms of the lowest datalog histogram (40-59 beats/min) increased from 0% to 15.4% +/- 0.9% of paced beats. Correlation between the patients' 24-hour diary and Holter recordings showed that the pacing rates during sleep were consistently lower than when the patients were awake and active. This was also the case with a patient whose nocturnal and daily routine was intentionally altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Septal short atrioventricular delay pacing: additional hemodynamic improvements in heart failure.

Controversy exists as to whether short AV delay pacing is beneficial in left ventricular dysfunction with the studies performed coming to disparate conclusions. The right ventricular apical pacing previously studied results in asynchronous contraction and relaxation sequences and may limit the potential benefits of short AV delay pacing. In this study the hemodynamic effects of septal (resulting in a more physiological activation sequence) and apical right ventricular activation were compared in 15 patients with heart failure. VDD pacing with AV delays of 50, 100, and 150 msec was evaluated. Apical VDD pacing did not increase the cardiac output significantly, 4.1 +/- 0.75 to 4.45 +/- 0.74 L/min, whereas septal VDD pacing increased the cardiac output to 4.86 +/- 0.79 L/min (P = 0.037). Apical pacing increased the cardiac output in 10 patients and septal pacing in 11 patients. We conclude that selected patients with ventricular dysfunction benefit from short AV delay pacing. Septal ventricular activation confers significant hemodynamic improvements over apical activation.

Hemodynamic and metabolic effects of paced linkage following heterotopic cardiac transplantation.

BACKGROUND AND PURPOSE: Heterotopic cardiac transplantation is a valuable surgical technique that maximizes the use of donor organs. However, recipient heart function may decline steadily postoperatively with resulting clinical deterioration. Paced linkage has the potential of reducing afterload and enhancing coronary flow of both hearts, thereby improving recipient- and donor-heart function. This may have long-term as well as short-term benefits. METHODS AND RESULTS: The study was performed on 11 heterotopic transplant recipients. The two hearts were linked with a pacemaker (paced linkage) to produce recipient heart systole during different periods of donor-heart diastole. The recipient ventricular contraction was timed to occur during early, mid, and late diastole of the donor heart. Hemodynamic baseline measurements were compared with the optimal counterpulsated data. Paced linkage produced significant improvements in total cardiac output, 5.0 +/- 0.9 compared with baseline 4.5 +/- 0.8 L/min (P = .021); recipient coronary sinus flow, 278 +/- 145 versus 186 +/- 108 mL/min (P = .022); and aortic systolic pressure, 135 +/- 27 versus 123 +/- 27 mm Hg (P = .005). There was an overall improvement in systolic ventricular performance in the recipient heart when pace linked, as evidenced by a significant increase in left ventricular systolic pressure of 118 +/- 36 compared with the baseline value of 108 +/- 33 mm Hg (P = .016), an increase in ejection period from 174 +/- 30 versus 203 +/- 48 (P = .046), and a decrease in the pre-ejection period of 147 +/- 37 when paced versus 181 +/- 39 milliseconds (P = .013). The metabolic studies showed a significant decrease in hypoxanthine release from a baseline level of 0.4 mumol/L to a paced value of -0.06 mumol/L (P = .002); these very low values would suggest that there is no evidence of ischemia. Hemodynamic changes in the donor heart included a significant reduction in the left ventricular end-diastolic pressure from 6.8 +/- 4.4 versus baseline of 10.5 +/- 5.8 mm Hg (P = .029) and in maximum -dP/dT from 3.2 +/- 1.7 versus baseline of 2.1 +/- 1.1. CONCLUSIONS: Paced linkage after heterotopic cardiac transplant produces significant functional improvements in both hearts. Permanent pacemaker implantation may sustain these acute benefits and prevent the premature deterioration of the recipient heart.

Postoperative hemodynamic improvement with paced linkage of the donor and recipient hearts following heterotopic cardiac transplantation.

It has been shown that following heterotopic heart transplantation the recipient left ventricle ejects more effectively when it contracts out of phase with the donor left ventricle. However, this is rarely the situation, as the two hearts beat independently of one another and the denervated donor heart tends to beat faster than the recipient. In this study the hemodynamic effects of connecting the two hearts by an external temporary dual-chamber pacemaker were evaluated. The donor right ventricle was sensed and the recipient right atrium paced after a timed delay. The delay was adjusted so that recipient systole coincided with donor diastole. Eleven patients were studied in the first postoperative day. Pacing resulted in an improvement in cardiac output from 5.0 to 5.6 l/min (p = 0.003) and a reduction in pulmonary capillary wedge pressure from 16 to 12 mmHg (p = 0.0035). This was associated with a 35% reduction in inotrope requirements. It is concluded that sequential pacing of the two hearts is a useful adjunct to inotropic support in the postoperative period.

Are we being driven to two sensors?: clinical benefits of sensor cross-checking.

Sensor cross-checking within dual sensor rate responsive pacemakers is designed to reduce the incidence of inappropriate rate response. We describe a patient in whom sensor cross-checking prevented the occurrence of angina during automotive transport.