Right ventricular pressure overload during acute lung injury: Cardiac mechanics and the pathophysiology of right ventricular systolic dysfunction

Right ventricular (RV) pressure overload (PO) accompanying acute lung injury is associated with a poor prognosis. To determine if RV ischemia (RVI) is responsible for RV failure (RVF) during acute PO induced by an acute lung injury, a group of eight dogs was studied with the pericardia open after instrumentation with RV, left ventricular (LV), and pulmonary artery (PA) Millar catheters, a PA thermodilution catheter, an aortic fluid-filled catheter, and RV and LV septal-free wall segment length crystals. The animals were studied during baseline, and after infusing glass beads into the right atrium sufficient to first double the PA pressure (PAP), then triple the PAP, and finally to produce RVF (decreased cardiac output with increased RV preload). Transmural RV biopsies were obtained at each phase for adenosine triphosphate and creatine phosphate (CP) assays. To determine the mechanism of RVI, a second group of nine dogs was studied (with the pericardia closed) at baseline, after a doubling of PAP and during RVF. Right ventricular myocardial blood flow was determined by a microsphere technique at each phase and was correlated with the determinants of RV myocardial O₂ demand and supply. In the open pericardia group, RVF, but not doubling or tripling of PAP, was associated with a decrease in CP to 50% of baseline conditions, confirming RVI (4.82 ± 3.67 versus 10.39 ± 3.94 μmol/gm wet weight; P < .005). In the closed pericardia group, RV myocardial blood flow increased in response to myocardial O₂ demands (multiple R = .69 for endocardial and .64 for epicardial flow; P < .05), although the ratio for total RV blood flow to myocardial O₂ demand ratio (planimetered area beneath RV pressure tracing) decreased (4.88 ± 2.76 versus 2.08 ± 2.14; P < .05). In both groups of dogs, RVF was associated with a similar decrease in LV end diastolic segment length or preload (17% in open group and 10% in closed group; P = NS between groups) and stroke work. From these observations, we conclude that after an acute lung injury, RVPO induces RVF because RV myocardial O₂ demand outstrips RV myocardial O₂ supply. Coincidentally with RVF, LV function is depressed on a preload-mediated basis independent of the pericardium, suggesting a dominant “series” interaction between both ventricles. These observations suggest that therapy in patients with acute lung injury is better aimed at increasing RV myocardial blood flow and RV function.     

Serial Doppler echocardiographic assessment of left and right ventricular performance after a first myocardial infarction.

We sought to investigate the relation between left ventricular (LV) and right ventricular (RV) function assessed with the Doppler-derived myocardial performance index (MPI), to assess serial changes, and to investigate the prognostic value of biventricular assessment of cardiac function after a first myocardial infarction (MI). To do so, serial Doppler echocardiography was performed in 77 consecutive patients with a first MI. Right ventricular MPI correlated significantly with LV MPI (r = 0.51, P <.0001). In patients with echocardiographic signs of RV MI, the RV MPI was significantly higher (0.59 +/- 0.18 versus 0.44 +/- 0.19, P =.001), whereas no difference in LV MPI was seen (0.55 +/- 0.19 versus 0.56 +/- 0.13, P = not significant). Right ventricular MPI showed a rapid normalization during follow-up, whereas LV MPI did not decrease. During follow-up, 23 patients died of cardiac causes or were readmitted because of worsening heart failure. Multivariate Cox analysis indicated LV MPI (relative risk 4.9 [95% CI 1.8-13.5], P =.002) and RV MPI (relative risk 3.8 [1.3-17.0], P =.01) to be predictors of cardiac events. Thus the RV MPI is frequently abnormal after a first MI but normalizes rapidly on follow-up, and biventricular assessment of cardiac function may improve the prognostic accuracy compared with LV assessment alone.     

Left ventricular geometry during intermittent positive pressure ventilation in dogs

We have analyzed how regional left ventricular (LV) performance may contribute to global LV performance during a single intermittent positive pressure ventilation (IPPV) respiratory cycle using chronically instrumented dogs with endocardial piezoelectric crystals in the three orthogonal axes, anterior-posterior (AP), septal-lateral freewall (SL), and long axis (LA) dimensions (D). Right ventricular (RV) SLD and aortic flow were also measured. Changes in LV geometry were evaluated during IPPV at two respiratory rates (10 and 20 breaths/min) and during inferior vena caval (IVC) occlusion since a change in systemic venous return is a major component of an IPPV inspiration. During an IPPV inspiration the RV SL end-diastolic D decreased, while the LV AP end-diastolic D increased (P < .01) and LV SL end diastolic D decreased (P < .001). LV end-diastolic and end-systolic volumes tended to increase during early inspiration and then diminished to an early expiratory minimum (P < .05) associated with early expiratory minimum stroke volumes and measured aortic flows (P < .02). In contrast, during IVC occlusion, the LV SL end-diastolic D initially increased while the AP end-diastolic D was falling. Thus, entirely different changes in LV end diastolic geometry result from IVC occlusion and lung inflation. These studies suggest a common factor of cardiac compression by the lung during inspiration altering diastolic intraventricular distribution of the LV preload and raise the question of whether respiratory-induced changes in LV geometry may independently modulate LV systolic pump function.     

Are biventricular systolic functions impaired in patient with coronoray slow flow? A prospective study with three dimensional speckle tracking

The newly developed three dimensional speckle-tracking echocardiography (3D-STE) technology provides quick and comprehensive quantitative assessment of biventricular myocardial dynamics. The impact of coronary slow flow phenomenon (CSFP) on biventricular functions has not been comprehensively evaluated using this new technology. Therefore, the aim of this study was to evaluate the effects of CSFP on biventricular systolic functions using 3D-STE. Forty patients with CSFP and otherwise normal coronary arteries (NCAs) and 40 age- and sex-matched controls with normal coronary angiograms (CAGs) were prospectively enrolled. Biventricular systolic function was evaluated by 3D-STE. Left ventricular (LV) global longitudinal, circumferential and radial strains, ejection fraction (EF) were significantly lower and LV end-systolic volume (ESV) was significantly higher in the CSFP group compared to the control group. There were no significant differences in LV mass, LV end-diastolic volume (EDV) or LV stroke volume (SV). Additionally, Right ventricular (RV) free wall, septal wall and global longitudinal strains, and RV EF were significantly lower in the CSFP group, but there were no significant differences in RV EDV, ESV and RV SV. The present study demonstrated that CSFP has a notable negative effect on not only 3D strain parameters but also biventricular EF. There was a strong correlation between the strain parameters of the affected vessel’s myocardial area and the TIMI frame count of same vessel.     

Right ventricular afterload mismatch during acute pulmonary hypertension and its treatment with dobutamine: A pressure segment length analysis in a canine model

The purpose of this study was twofold. First, we wished to determine if right ventricular ischemia initiates the development of a decrease in cardiac output during acute pulmonary hypertension and, second, we wished to determine the hemodynamic and metabolic effects of dobutamine once the decreased cardiac output state had occurred. Six open chest and open pericardium dogs were studied after instrumentation with right and left ventricular (RV and LV, respectively), and pulmonary artery (PA) Millar catheters, a PA thermodilution catheter, and RV and LV segment length crystals. Measurements were taken before and after the administration of sufficient glass bead emboli to first triple the PA pressure and then to decrease the cardiac output by approximately 20% compared with the cardiac output in the preceding condition. Measurements were repeated after infusing dobutamine at 5 μg/kg/min for 20 minutes and then at 10 μg/kg/min for 20 minutes. In addition to hemodynamic measurements, RV tissue biopsies were obtained for adenosine triphosphate (ATP) and creatine phosphate (CP) determinations at each stage. Our results demonstrated that the occurrence of a modest decrease in cardiac output during acute pulmonary hypertension was not associated with any decrease in either ATP or CP level. Low-dose dobutamine increased cardiac output by increasing heart rate and stroke volume. Higher dose dobutamine decreased both RV preload and afterload which culminated in a reduction in cardiac output in four of the six animals; however, mean cardiac output actually increased. Neither dose range affected RV ATP or CP. We conclude that reduced cardiac output during pulmonary hypertension is secondary to RV afterload mismatch, not ischemia. Low-dose dobutamine can increase cardiac output by increasing stroke volume and chronotropic effects. Although high-dose dobutamine can increase cardiac output further, it also has significant effects on RV preload and afterload which are potentially deleterious.     

The right ventricle: interaction with the pulmonary circulation

The primary role of the right ventricle (RV) is to deliver all the blood it receives per beat into the pulmonary circulation without causing right atrial pressure to rise. To the extent that it also does not impede left ventricular (LV) filling, cardiac output responsiveness to increased metabolic demand is optimized. Since cardiac output is a function of metabolic demand of the body, during stress and exercise states the flow to the RV can vary widely. Also, instantaneous venous return varies widely for a constant cardiac output as ventilatory efforts alter the dynamic pressure gradient for venous return. Normally, blood flow varies with minimal changes in pulmonary arterial pressure. Similarly, RV filling normally occurs with minimal increases in right atrial pressure. When pulmonary vascular reserve is compromised RV ejection may also be compromised, increasing right atrial pressure and limiting maximal cardiac output. Acute increases in RV outflow resistance, as may occur with acute pulmonary embolism, will cause acute RV dilation and, by ventricular interdependence, markedly decreased LV diastolic compliance, rapidly spiraling to acute cardiogenic shock and death. Treatments include reversing the causes of pulmonary hypertension and sustaining mean arterial pressure higher than pulmonary artery pressure to maximal RV coronary blood flow. Chronic pulmonary hypertension induces progressive RV hypertrophy to match RV contractility to the increased pulmonary arterial elastance. Once fully developed, RV hypertrophy is associated with a sustained increase in right atrial pressure, impaired LV filling, and decreased exercise tolerance. Treatment focuses on pharmacologic therapies to selectively reduce pulmonary vasomotor tone and diuretics to minimize excessive RV dilation. Owning to the irreversible nature of most forms of pulmonary hypertension, when the pulmonary arterial elastance greatly exceeds the adaptive increase in RV systolic elastance, due to RV dilation, progressive pulmonary vascular obliteration, or both, end stage cor pulmonale ensues. If associated with cardiogenic shock, it can effectively be treated only by artificial ventricular support or lung transplantation. Knowing how the RV adapts to these stresses, its sign posts, and treatment options will greatly improve the bedside clinician’s ability to diagnose and treat RV dysfunction.     

Physiology of Cardiac Pacing in Children: The Importance of the Ventricular Pacing Site

Children with congenital or acquired atrioventricular block are provided with ventricular rate support from a pacing lead that traditionally is positioned at the right ventricular (RV) apex. However, RV apical pacing causes dyssynchronous electrical activation and left ventricular (LV) contraction, resulting in decreased LV function. Chronic RV apical pacing leads to deterioration of LV function and morphology, resulting in cardiac failure in approximately 7% of children. This review describes the pathophysiology of pacing-induced dyssynchronous LV activation and contraction, especially as a result of chronic RV apical pacing. Furthermore, this review provides an overview of the possible alternative pacing sites, such as the RV outflow tract, His-bundle, LV apex, and biventricular pacing.     

Multisite Pacing for End-Stage Heart Failure: Early Experience

Our objective was to improve hemodynamics by synchronous right and left site ventricular pacing in patients with severe congestive heart failure (CHF). Previous studies reported a benefit of dual chamber pacing with a short AV delay in patients with severe CHF. Other works, however, show contradictory results. Deleterious effects due to a desynchronization of right (RV) and left ventricular (LV) contractions have been suggested. This study included eight subjects with widened QRS and end-stage heart failure despite maximal medical therapy, who refused, or were not eligible to undergo heart transplantation. Each patient underwent a baseline, invasive hemodynamic evaluation with insertion of three temporary leads to allow different pacing configurations, including RV apex and outflow tract pacing, and biventricular pacing between the RV outflow tract and LV and RV apex and LV. According to the results of this baseline study, the configuration of preexistent pacemakers was modified or new systems were implanted to allow biventricular pacing, which, in patients with sinus rhythm, was atrial triggered. Biventricular pacing increased the mean cardiac index (CI) by 25% (from a baseline of 1.83 ± 0.30 L/min per m², P < 0.006), decreased the mean V wave by 26% (from a baseline of 36 ± 12 mmHg, P < 0.004), and decreased pulmonary capillary wedge pressure by 17% (from a baseline of 31 ± 10 mmHg, P < 0.01). Four patients died (1 preoperatively, 1 intraoperatively, 2 within 3 months, and 1 of a noncardiac cause). The four surviving patients have clinically improved from New York Heart Association Functional Class IV to Class II. In these survivors, CI decreased by 15% (P < 0.007) when multisite pacing was turned off during follow-up. In patients with end-stage heart failure, multisite pacing may be associated with a rapid and sustained hemodynamic improvement.     

Comparison between acute hypoxia-induced and mechanically-induced pulmonary artery hypertension on the hemodynamics, myocardial contractility and regional blood flow in dogs

Summary— Two groups of eight anesthetized dogs with pulmonary artery hypertension (PAH) were compared. PAH was induced by submitting one group (HP) to hypoxia (FiO2 range: 6–10%) and the other group (ME) to microemboli through glass microbead injection into the pulmonary circulation. Hypoxia-induced PAH was moderate (PAP: +65%; PVR: + 152%) contrasting with marked PAH after microbead injection (PAP: +190%; PVR: +389%). For similar effects on left ventricular contractility (LV dP/dt max and segmental myocardial shortening), heart rate and systemic vascular resistance, left ventricular end-diastolic pressure showed significant differences between the two groups (HP group: +75%, ME group: −9%), and so did left ventricular end-diastolic length (HP: +9%, ME: −11%). Thus, contrary to the injection of microbeads, hypoxia did not give rise to any pulmonary barrier, and consequently the changes in cardiac output (HP: +19%, ME: −15%) and hepatic blood flow (HP: +383%, ME: −77%) were significantly different. Hypoxia, and not microbead injection, was responsible for systemic hypertension (MAP: +34% and −4%, respectively). The microbead model resulted in a significantly higher PVR/SVR ratio compared to the hypoxic model (HP: 0.14, ME: 0.41). Hypoxia increased left and right myocardial blood flows whereas microbead injection affected only right ventricular blood flow, leading to significantly different RV/LV endocardial perfusion ratios (HP: +10%, ME: +98%). We conclude that microbead-induced PAH is more appropriate than hypoxia-induced PAH for hemodynamic and pharmacological studies.     

Impact of different pacing modes on left ventricular contractility following cardiopulmonary bypass

BACKGROUND: Acute left ventricular (LV) dysfunction after cardiopulmonary bypass (CBP) is a serious complication in cardiac surgery. The aim of this study was to investigate the effect of different epicardial pacing modes on LV contractility and changes of myocardial oxygen extraction (MVO(2)) following CPB in an animal model. The utility of conductance catheter measurement versus left ventricular outflow tract mean systolic acceleration (LVOT(Acc)) for quantification of LV function was evaluated. METHODS: Fourteen piglets underwent median sternotomy and CPB for 90 minutes, myocardial ischemia for 60 minutes, and reperfusion for 30 minutes. Different pacing modes were obtained before and after CPB to investigate changes in LV function. LV Function was quantified by end-systolic-pressure-volume relationships (ESPVR) as measured by the conductance catheter method and by LVOT(Acc) obtained from transepicardial echocardiographic studies. RESULTS: LV contractility improved significantly by biventricular and atrial pacing compared with natural sinus rhythm (SR). MVO(2) remained stable or even decreased with biventricular pacing after surgery compared with SR. Right ventricular pacing resulted in poor LV-function with a rise of MVO(2). LVOT(Acc) showed a strong correlation to invasively measured ESPVR. CONCLUSION: Postoperative biventricular pacing was associated with an improved LV contractility without rise of MVO(2) compared with SR and atrial pacing. At termination of CPB, this appears to facilitate the management of LV failure and potentially may reduce the need for inotropic support, additionally protecting myocardial metabolism. The echocardiographic assessment of LVOT(Acc) was a simple and reliable as well as effective method to quantify LV contractility and showed a good correlation with the more invasive conductance catheter.     

Bifocal Right Ventricular Cardiac Resynchronization Therapies in Patients with Unsuccessful Percutaneous Lateral Left Ventricular Venous Access

Biventricular cardiac resynchronization therapy (CRT) with a lateral left ventricular (LV) lead cannot always be achieved. We report a single center experience of CRT utilizing a protocol that specifically required the implantation of a bifocal right ventricular (RV) lead system when lateral LV pacing could not be achieved. Consecutive candidates for CRT were included in the study. If strict criteria for lateral LV pacing were not met, they underwent implantation of a bifocal RV lead system with two 7F, active fixation leads, one placed septally at the apex, and the other in the high septal outflow tract. All patients were followed for 12 months and the two groups were compared. A biventricular (BiV) stimulation system was implanted in 44 patients, and a bifocal RV system in six. The demographic characteristics of the two groups were similar. Both groups experienced a similar improvement in functional capacity, increase in 6 minutes walking distance, and decreased need for hospitalizations. The mean increase in LV ejection fraction was 11% in the bifocal RV group versus 10% in the BiV group. Though the tissue Doppler indices of LV synchrony improved earlier in the BiV group, (19% vs 10%) the improvement was similar in both groups at 6 months (23% vs 20%). The clinical improvements conferred by CRT can be matched by a bifocal RV system in selected patients. This alternate approach should be considered when implantation of a LV lateral lead was unsuccessful.     

Optical Mapping Technique Applied to Biventricular Pacing:

GARRIGUE, S., et al .: Optical Mapping Technique Applied to Biventricular Pacing: Potential Mechanisms of Ventricular Arrhythmias Occurrence. Although it has been suggested that multisite ventricular pacing alleviates heart failure by restoring ventricular electrical synchronization, the respective roles of voltage output, interventricular delay, and pacing sites in the development of ventricular arrhythmias occurrence have not been studied during biventricular pacing or LV pacing. Voltage-sensitive dye was used in eight ischemic Langerdorff-perfused guinea pig hearts to measure ventricular activation times and examine conduction patterns during multisite pacing from three RV and four LV sites. The hearts were stained with di-4-ANEPPS and mapped with a   16 × 16   photodiode array at a resolution of 625 μm per diode. Isochronal maps of RV and LV activation were plotted. Ischemia was produced by gradually halving the perfusion output over 5 minutes. Pacing the RV apex and the base of the LV anterior wall was associated with the most homogeneous and rapid activation pattern (   28 ± 9   vs   41 ± 12   ms with the other configurations, P < 0.01), and no inducible arrhythmia. In six hearts, ventricular tachycardia could be induced when pacing from the right and left free walls with 20 ms of interventricular delay, at six times the pacing threshold output. In four hearts, simultaneous RV and LV pacing at high voltage output induced ventricular fibrillation with complex three-dimensional propagation patterns, independently of the pacing sites. During biventricular pacing with ischemia, pacing at high voltage output with a long interventricular delay is likely to induce ventricular arrhythmias, particularly when left and right pacing results in a conduction pattern orthogonal to the ventricular myocardial fibers orientation. PACE 2003; 26[Pt. II]:197–205)     

Increasing left ventricular pacing output decreases interventricular conduction time in patients with biventricular pacing systems

OBJECTIVE: To evaluate the effect of increasing LV pacing output on interventricular timing in patients with biventricular pacing systems. BACKGROUND: Clinical improvement with biventricular pacing is likely related to reduction in ventricular dysynchrony in patients with cardiomyopathy. We hypothesized that increasing left ventricular pacing output would reduce interventricular conduction time and could affect ventricular synchrony. METHODS: Forty-two sequential patients with biventricular pacing systems that permitted independent LV pacing were selected at the time of routine device interrogation. The interval between LV pacing stimulus and onset of the RV electrogram was measured during LV pacing at capture threshold and at maximum pacing output for each patient. RESULTS: The average time from LV pacing stimulus to right ventricular electrogram onset was 142.5 +/- 32.5 ms (range 90-230 ms) at threshold and 132.3 +/- 30.4 ms (range 90-220 ms) at maximum pacing output, with a mean decrease in conduction time of 10.2 +/- 10.9 ms (range 0-45 ms). There was significantly greater interventricular conduction shortening with increased pacing output in patients with ischemic cardiomyopathy compared to others (14.9 +/- 11.9 ms vs 4.0 +/- 4.6 ms; P < 0.01). CONCLUSIONS: Conduction time from LV to RV shortens as LV pacing output is increased. This effect is seen to a greater degree in patients with ischemic cardiomyopathy, possibly related to the presence of myocardial scar near the pacing electrode. Further investigation is needed to assess the clinical outcomes related to this new method for optimizing resynchronization therapy.     

Diagnostic and prognostic value of right ventricular strain in patients with pulmonary arterial hypertension and relatively preserved functional capacity studied with echocardiography and magnetic resonance

Right ventricular (RV) dysfunction harbingers adverse prognosis in pulmonary arterial hypertension (PAH). Although conventional two-dimensional echocardiography (2DE) is limited for RV systolic function quantitation, RV strain can be a useful tool. The diagnostic and prognostic impact of 2DE speckle-tracking RV longitudinal strain was evaluated, including other 2DE systolic indexes, in a group of PAH patients without severe impairment of functional capacity, chronic pulmonary thromboembolism or left ventricular dysfunction. Sixty-six group I PAH patients, 67?% NYHA functional class I or II (none in IV) were studied by 2DE to obtain: RV fractional area change, tricuspid annular plane systolic excursion, RV myocardial performance index, tissue Doppler tricuspid annulus systolic velocity. Global, free wall (RVFreeWSt) and septal RV longitudinal systolic strain were obtained. RV ejection fraction by cardiac magnetic resonance (CMR-RVEF) was also assessed. All patients were followed up to 3.9 years (mean 3.3 years). Combined endpoints were hospitalization for worsening PAH or cardiovascular death. Among all the 2DE indexes of RV systolic function, RVFreeWSt exhibited the best correlation with CMR-RVEF (r = 0.83; p?<?0.005). Combined endpoints occurred in 15 (22.7?%) patients (6 hospitalizations and 9 deaths). Multivariate analysis identified RVFreeWSt ≤?14?% as the only 2DE independent variable associated with combined endpoints [HR 4.66 (1.25–17.37); p?<?0.05]. We conclude that RVFreeWSt may be a suitable non-geometric 2DE surrogate of CMR-RVEF in PAH patients, constituting a powerful independent predictor of long-term outcome in this cohort with relatively preserved functional capacity.     

Reproducibility of peak filling and peak emptying rate determined by cardiovascular magnetic resonance imaging for assessment of biventricular systolic and diastolic dysfunction in patients with pulmonary arterial hypertension

Right ventricular (RV) and left ventricular (LV) diastolic stiffness may be independent contributors to disease progression in pulmonary arterial hypertension (PAH). The aims of this study are to assess reproducibility of peak emptying rate (PER) and early diastolic peak filling rate (PFR) for both the RV and the LV in PAH and study their relationship to stroke volume (SV). Triple weekly repetition of 20 (totalling 60) cardiovascular magnetic resonance (CMR) scans, were done on 10 patients with PAH and 10 healthy controls. RV and LV volumes were measured over the full cardiac cycle. PER and PFR were calculated as the first derivative of the time–volume relationship in both the RV and the LV and indexed to body surface area. Reproducibility and the relation to SV were studied in a mixed model. PFR was lower in PAH in both the RV (PAH?=?170 mL/m²/s, controls?=?236 mL/m²/s [p?<?0.01]) and in the LV (PAH?=?209 mL/m²/s, controls?=?311 mL/m²/s [p?<?0.01]). PERs were not significantly different between patients and controls. Reproducibility of PER and PFR was high. A trial targeting normalization of PFR requires a total sample size of <?20. PER and PFR in both ventricles were strongly associated with stroke volume (all four: p?<?0.01). Biventricular diastolic dysfunctions are strongly associated with stroke volume, and CMR can quantify them with high reproducibility, enabling small sample sizes for trials of therapies targeting diastolic dysfunction to increase survival.     

超声心动图评价起搏模式及起搏部位对心脏再同步化治疗效果的影响

目的：评价超声心动图在心力衰竭患者心脏再同步化治疗（cardiac resynchronizatio therapy，CRT）中的应用价值，探讨起搏模式及起搏部位对其产生的影响。方法：34例患者植入双室起搏器后随机进行4种不同模式起搏（双腔起搏，左室起搏，右室起搏和不起搏即窦性心律状态）。行常规超声心动图及二维彩色组织多普勒（Doppler tissue imaging，DTI）检查，测量左室射血分数（LVEF）、每搏输出量（Sv）、节段心肌作功指数（MPIr）和每个节段心电图QRS波起始至该节段收缩达峰时间（Ts），并比较左室电极放置在不同位置对心功能的影响。结果：左室起搏和双腔起搏提高SV（均P〈0．02）和LVEF（均P〈0.001）。左室起搏和双腔起搏下左室节段MPIr改善（均P〈0．0001），下壁和前壁基底段Ts差缩短（均P〈0．0001）。电极放置在心脏侧后静脉或侧静脉时SV、LVEF和Ts较后静脉或前静脉明显改善。结论：左室起搏和双腔起搏可明显改善心力衰竭患者的心功能。超声心动图可以无创评价CRT治疗效果，并随访预后。     

二维超声心动图评价肺动脉高压患者心脏结构与功能关系的临床研究

目的：探讨心室间相互作用的机制。方法：用超声方法测量了４２例肺动脉高压患者的心功能和心脏结构参数,并与右心导管术检查结果做比较。结果：肺动脉高压患者右心输出量增加,但射血分数明显低于正常对照组,而左室射血分数在正常范围。二尖瓣及三尖瓣均表现为Ｅ峰流速降低,Ｅ／Ａ＜１及心室等容舒张时间间期（ＩＶＲＴ）明显延长,但二尖瓣Ａ峰流速变化不明显,而三尖瓣Ａ峰流速明显增高。室间隔左移,使左室内径减小,且与肺动脉压升高的程度相关显著,整个心动周期左室偏心指数（ＥＩ）明显增大（ｐ＜０．００１）。右室游离壁明显增厚,室间隔及左室游离壁也增厚（ｐ＜０．０１;ｐ＜０．０１）。结论：肺动脉高压患者右室收缩及舒张功能均减低,而左室收缩功能正常,主要是舒张功能降低且与舒张期左室几何形状即室间隔的移位及肺动脉压增高的程度有关     

Ventricular interaction: from bench to bedside

Decreased right ventricle (RV) output results in decreased left ventricle end-diastolic volume (LVEDV) and output by series interaction. Direct ventricular interaction may also have a major effect on LV function. Thus, decreased LVEDV caused by reduced RV output may be further reduced by a leftward septal shift and pericardial constraint. This has been shown to be true in acute and chronic pulmonary hypertension and is now also apparent in severe congestive heart failure. The use of intracavitary LV end-diastolic pressure (LVEDP) to assess LVEDV is inappropriate if pressure surrounding the LV is increased: the surrounding pressure should be subtracted from LVEDP to calculate the effective distending (transmural) pressure which governs preload. If the surrounding pressure increases more than LVEDP, transmural LVEDP and LVEDV will decrease despite the increased LVEDP. Thus, the use of filling pressure to reflect changes in LVEDV has led to erroneous conclusions regarding changes in myocardial compliance and contractility. It is now clear that volume loading may reduce LVEDV and stroke work in pulmonary embolism, chronic lung disease and severe congestive heart failure despite increased LVEDP. The decreased stroke work is a result of reduced LV preload, not decreased contractility as would be suggested if filling pressure is used to reflect preload.     

Site‐Specific Differences in Latency Intervals during Biventricular Pacing: Impact on Paced QRS Morphology and Echo‐Optimized V‐V Interval

Objective: To investigate differences in latency intervals during right ventricular (RV) pacing and left ventricular (LV) pacing from the (postero‐)lateral cardiac vein in cardiac resynchronization therapy (CRT) patients and their relationship to echo‐optimized interventricular (V‐V) intervals and paced QRS morphology. Methods: We recorded digital 12‐lead electrocardiograms in 40 CRT patients during RV, LV, and biventricular pacing at three output settings. Stimulus‐to‐earliest QRS deflection (latency) intervals were measured in all leads. Echocardiographic atrioventricular (AV) and V‐V optimization was performed using aortic velocity time integrals. Results: Latency intervals were longer during LV (34 ± 17, 29 ± 15, 28 ± 15 ms) versus RV apical pacing (17 ± 8, 15 ± 8, 13 ± 7 ms) for threshold, threshold ×3, and maximal output, respectively (P < 0.001), and shortened with increased stimulus strength (P < 0.05). The echo‐optimized V‐V interval was 58 ± 31 ms in five of 40 (12%) patients with LV latency ≥ 40 ms compared to 29 ± 20 ms in 35 patients with LV latency < 40 ms (P < 0.01). During simultaneous biventricular pacing, four of five (80%) patients with LV latency ≥ 40 ms exhibited a left bundle branch block (LBBB) pattern in lead V₁ compared to three of 35 (9%) patients with LV latency < 40 ms (P < 0.01). After optimization, all five patients with LV latency ≥ 40 ms registered a dominant R wave in lead V₁. Conclusions: LV pacing from the lateral cardiac vein is associated with longer latency intervals than endocardial RV pacing. LV latency causes delayed LV activation and requires V‐V interval adjustment to improve hemodynamic response to CRT. Patients with LV latency ≥ 40 ms most often display an LBBB pattern in lead V₁ during simultaneous biventricular pacing, but a right bundle branch block after V‐V interval optimization. (PACE 2010; 1382–1391)     

Right ventricular function in acute disease states: pathophysiologic considerations

In critically ill patients, alterations in pulmonary vasomotor tone profoundly influence right ventricular (RV) function. An increase in end-diastolic volume (EDV) follows elevations in the RV afterload, this increase in preload probably subserving the increased RV stroke work (SW) required to ensure unchanged RV pump function. The maintenance of a normal left ventricular (LV) preload is essential in the cardiovascular adaptation to an acute illness. With volume overload of the RV consequent upon pulmonary artery hypertension (PAH), leftward septal shift occurs and reduces LV diastolic compliance. With extremely high levels of RV loading conditions, a depression in RV contractility and reduced RV pump function are eventually seen, both of which then become partially responsible for LV pump failure. Hence, abnormalities in RV function will have a marked clinical influence on the circulatory response seen in critically ill patients. Future investigation should be directed toward the effects of augmenting or improving RV function with pharmacologic agents in this patient population.