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Paul Steendijk

Publications and source records attributed to Paul Steendijk.

At least 19 recordsLinked to original sources
PubMed2006

Impact of viability and scar tissue on response to cardiac resynchronization therapy in ischaemic heart failure patients.

AIMS: At present, 20-30% of patients do not respond to cardiac resynchronization therapy (CRT). In this study, the relation between the extent of viable myocardium and scar tissue vs. response to CRT was evaluated. In addition, the presence of scar tissue in the left ventricular (LV) lead position was specifically related to response to CRT. METHODS AND RESULTS: A total of 51 consecutive patients with ischaemic heart failure and substantial LV dyssynchrony undergoing CRT were included. All patients underwent gated SPECT before CRT implantation to determine the extent of scar tissue and viable myocardium. Clinical and echocardiographic parameters were assessed at baseline and after 6 months of CRT. The results demonstrated direct relations between the response to CRT and the extent of viable myocardium and scar tissue. In addition, the 15 patients (29%) with transmural scar tissue (< 50% tracer activity) in the region of the LV pacing lead showed no improvement after 6 months of CRT. CONCLUSION: The extent of scar tissue and viable myocardium were directly related to the response to CRT. Furthermore, scar tissue in the LV pacing lead region may prohibit response to CRT. Evaluation for viability and scar tissue may be considered in the selection process for CRT.

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PubMed2006

Relative merits of M-mode echocardiography and tissue Doppler imaging for prediction of response to cardiac resynchronization therapy in patients with heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

M-mode echocardiography (using the septal-to-posterior wall motion delay [SPWMD]) and color-coded tissue Doppler imaging (TDI; using the septal-to-lateral delay in peak systolic velocity) have been proposed for assessment of left ventricular (LV) dyssynchrony and prediction of response to cardiac resynchronization therapy (CRT). In this study, a head-to-head comparison between M-mode echocardiography and color-coded TDI was performed for assessment of LV dyssynchrony and prediction of response to CRT. Consecutive (n = 98) patients with severe heart failure (New York Heart Association class III/IV), LV ejection fraction < or =35%, and QRS duration >120 ms underwent CRT. Before pacemaker implantation, LV dyssynchrony was assessed by M-mode echocardiography (SPWMD) and color-coded TDI (septal-to-lateral delay). At baseline and 6 months after implantation, clinical and echocardiographic parameters were evaluated. SPWMD measurement was not feasible in 41% of patients due to akinesia of the septal and/or posterior walls or poor acoustic windows. Conversely, the septal-to-lateral delay could be assessed in 96% of patients. At 6-month follow-up, 75 patients (77%) were classified as responders to CRT (improvement > or =1 New York Heart Association class). The sensitivity and specificity of SPWMD were lower compared with those of septal-to-lateral delay (66% vs 90%, p <0.05; 50% vs 82%, p = NS, respectively). In conclusion, LV dyssynchrony assessment was feasible in 59% of patients with M-mode echocardiography compared with 96% (p <0.05) when color-coded TDI was used. Color-coded TDI was superior to M-mode echocardiography for prediction of response to CRT.

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PubMed2006

Cardiac resynchronization therapy in patients with a narrow QRS complex.

OBJECTIVES: The purpose of this study was to evaluate the effects of cardiac resynchronization therapy (CRT) in heart failure patients with narrow QRS complex (<120 ms) and evidence of left ventricular (LV) dyssynchrony on tissue Doppler imaging (TDI). BACKGROUND: Cardiac resynchronization therapy is beneficial in selected heart failure patients with wide QRS complex (> or =120 ms). Patients with narrow QRS complex are currently not eligible for CRT, and the potential effects of CRT are not well studied. METHODS: Thirty-three consecutive patients with narrow QRS complex and 33 consecutive patients with wide QRS complex (control group) were prospectively included. All patients needed to have LV dyssynchrony > or =65 ms on TDI, New York Heart Association (NYHA) functional class III/IV heart failure, and LV ejection fraction < or =35%. RESULTS: Baseline characteristics, particularly LV dyssynchrony, were comparable between patients with narrow and wide QRS complex (110 +/- 8 ms vs. 175 +/- 22 ms; p = NS). No significant relationship was observed between baseline QRS duration and LV dyssynchrony (r = 0.21; p = NS). The improvement in clinical symptoms and LV reverse remodeling was comparable between patients with narrow and wide QRS complex (mean NYHA functional class reduction 0.9 +/- 0.6 vs. 1.1 +/- 0.6 [p = NS] and mean LV end-systolic volume reduction 39 +/- 34 ml vs. 44 +/- 46 ml [p = NS]). CONCLUSIONS: Cardiac resynchronization therapy appears to be beneficial in patients with narrow QRS complex and severe LV dyssynchrony on TDI, with similar improvement in symptoms and comparable LV reverse remodeling to patients with wide QRS complex. The current results need confirmation in larger patient cohorts.

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PubMed2006

Characterization of right ventricular function after monocrotaline-induced pulmonary hypertension in the intact rat.

We characterized hemodynamics and systolic and diastolic right ventricular (RV) function in relation to structural changes in the rat model of monocrotaline (MCT)-induced pulmonary hypertension. Rats were treated with MCT at 30 mg/kg body wt (MCT30, n = 15) and 80 mg/kg body wt (MCT80, n = 16) to induce compensated RV hypertrophy and RV failure, respectively. Saline-treated rats served as control (Cont, n = 13). After 4 wk, a pressure-conductance catheter was introduced into the RV to assess pressure-volume relations. Subsequently, rats were killed, hearts and lungs were rapidly dissected, and RV, left ventricle (LV), and interventricular septum (IVS) were weighed and analyzed histochemically. RV-to-(LV + IVS) weight ratio was 0.29 +/- 0.05 in Cont, 0.35 +/- 0.05 in MCT30, and 0.49 +/- 0.10 in MCT80 (P < 0.001 vs. Cont and MCT30) rats, confirming MCT-induced RV hypertrophy. RV ejection fraction was 49 +/- 6% in Cont, 40 +/- 12% in MCT30 (P < 0.05 vs. Cont), and 26 +/- 6% in MCT80 (P < 0.05 vs. Cont and MCT30) rats. In MCT30 rats, cardiac output was maintained, but RV volumes and filling pressures were significantly increased compared with Cont (all P < 0.05), indicating RV remodeling. In MCT80 rats, RV systolic pressure, volumes, and peak wall stress were further increased, and cardiac output was significantly decreased (all P < 0.05). However, RV end-systolic and end-diastolic stiffness were unchanged, consistent with the absence of interstitial fibrosis. MCT-induced pressure overload was associated with a dose-dependent development of RV hypertrophy. The most pronounced response to MCT was an overload-dependent increase of RV end-systolic and end-diastolic volumes, even under nonfailing conditions.

Animals↗
PubMed2006

Cardiac resynchronization therapy in patients with systolic left ventricular dysfunction and symptoms of mild heart failure secondary to ischemic or nonischemic cardiomyopathy.

Cardiac resynchronization therapy (CRT) is beneficial in selected patients with moderate to severe heart failure (New York Heart Association [NYHA] classes III to IV). Patients with mildly symptomatic heart failure (NYHA class II) are currently not eligible for CRT and the potential beneficial effects in these patients have not been well studied. Fifty consecutive patients in NYHA class II heart failure and 50 consecutive patients in NYHA classes III to IV (control group) were prospectively included. All patients had left ventricular (LV) ejection fraction 120 ms. The effects of CRT in NYHA class II patients were compared with the results obtained in both groups. The severity of baseline LV dyssynchrony (assessed with color-coded tissue Doppler imaging) was comparable between patients in NYHA class II versus those in NYHA classes III to IV (83+/-49 vs 96+/-51 ms, p=NS); resynchronization was achieved in all patients. NYHA class II patients showed a significant improvement in LV ejection fraction (from 25+/-7% to 33+/-10%, p<0.001) and reduction in LV end-systolic volume (from 168+/-55 to 132+/-51 ml, p<0.001) after CRT, similar to patients in NYHA classes III to IV. In addition, only 8% of NYHA class II patients had progression of heart failure symptoms. In conclusion, CRT had comparable effects in patients in NYHA class II and in NYHA classes III to IV heart failure in terms of LV resynchronization, improvement in LV ejection fraction, and LV reverse remodeling.

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PubMed2006

Coronary vasospasm-induced acute diastolic dysfunction in a patient with Raynaud's phenomenon.

We present the case of a patient with severe dyspnea and Raynaud's phenomenon. We could clarify, using invasive techniques including left ventricular conductance catheterization and coronary ergonovine provocation, that isolated diastolic dysfunction induced by coronary vasospasm were responsible for the symptoms. Systolic function was not affected. Short-term infusions with the prostacyclin analogue iloprost, known to act as a disease-modifying agent in patients suffering from Raynaud's phenomenon, led to an improvement of cardiac function. Thus, episodes of dyspnea in patients with Raynaud's phenomenon might be also interpreted as a coronary ischemia equivalent, which may belong to a visceral form of Raynaud's phenomenon and which are sensitive to iloprost infusions.

Coronary Vasospasm↗
PubMed2006

Right and left ventricular function after chronic pulmonary artery banding in rats assessed with biventricular pressure-volume loops.

In many patients with congenital heart disease, the right ventricle (RV) is subjected to abnormal loading conditions. To better understand the state of compensated RV hypertrophy, which could eventually progress to decompensation, we studied the effects of RV pressure overload in rats. In the present study, we report the biventricular adaptation to 6 wk of pulmonary artery banding (PAB). PAB resulted in an RV pressure overload to approximately 60% of systemic level and a twofold increase in RV mass (P < 0.01). Systemic hemodynamic parameters were not altered, and overt signs of heart failure were absent. Load-independent measures of ventricular function (end-systolic pressure-volume relation, preload recruitable stroke work relation, maximum first time derivative of pressure divided by end-diastolic volume), assessed by means of pressure-volume (PV) loops, demonstrated a two- to threefold increase in RV contractility under baseline conditions in PAB rats. RV contractility increased in response to dobutamine stimulation (2.5 microg.kg(-1).min(-1)) both in PAB and sham-operated rats in a similar fashion, indicating preserved RV contractile reserve in PAB rats. Left ventricular (LV) contractility at baseline was unaffected in PAB rats, although LV volume in PAB rats was slightly decreased. LV contractility increased in response to dobutamine (2.5 microg.kg(-1).min(-1)), both in PAB and sham rats, whereas the response to a higher dose of dobutamine (5 microg.kg(-1).min(-1)) was blunted in PAB rats. RV pressure overload (6 wk) in rats resulted in a state of compensated RV hypertrophy with preserved RV contractile reserve, whereas LV contractile state at baseline was not affected. Furthermore, this study demonstrates the feasibility of performing biventricular PV-loop measurements in rats.

Animals↗
PubMed2006

Time-varying elastance concept applied to the relation of carotid arterial flow velocity and ventricular area.

OBJECTIVE: In this study, the relationship V(f)AR, which was obtained from carotid blood-flow velocity (V(f)) and the cross-sectional area (A) of the left ventricle, was used to assess changes in left ventricular (LV) systolic performance as indicated by the LV pressure-volume relationship (PVR) and end-systolic LV elastance (E(es)). BACKGROUND: The relationship of maximum systolic V(f) as a surrogate for LV pressure and end-systolic LV area as a surrogate for end-systolic LV volume may allow for the estimation of LV elastance and ejection properties. METHODS: In 25 pigs, internal carotid V(f) was recorded by using continuous-wave Doppler mode. Echocardiographic measurements of A were continuously performed with an automated border detection system and combined with data for V(f) to display V(f)AR as a series of loop diagrams. These were shifted during acute preload reduction, and an index E'(es) was calculated by applying the time varying elastance concept to end-systolic V(f)AR. Simultaneously, E(es) was acquired by conductance catheter and micromanometer techniques. Comparisons of E'(es) and E(es) were made at various contractility levels obtained by the administration of dobutamine, 5 microg/kg/min, and esmolol, 40 to 60 mg, and at various cardiac load levels, obtained by a fluid bolus infusion or administration of a vasoconstrictor. RESULTS: Highly linear elastance curves (r >or= 0.85, p < 0.0001) were derived from both end-systolic V(f)AR and PVR. Correlation of E'(es) and E(es) revealed an almost linear function: E'(es) = 0.052 + 0.11 E(es) (r = 0.98, p < 0.0001). Administration of dobutamine increased E(es) from 5.8 +/- 3.04 mmHg/mL to 10.1 +/- 4.19 mmHg/mL (p < 0.05), and E('es) from 0.68 +/- 0.288 cm(2)/min/mL to 1.24 +/- 0.458 cm(2)/min/mL (p < 0.05). After administration of esmolol, E(es) and E'(es) both dropped significantly by 3.7 +/- 2.4 mmHg/mL and 0.44 +/- 0.15 cm(2)/min/mL, respectively. No load dependency of E'(es) was seen. Bland-Altman analysis revealed that the change in E'(es), which is required to predict a significant change in E(es), should exceed +16.9% or -13.1% of the preceding value. CONCLUSION: Application of the time-varying elastance concept on the relation of V(f) and LV area allows for the determination of an index E'(es) that may be used to estimate E(es).

Animals↗
PubMed2006

Hemodynamic effects of long-term cardiac resynchronization therapy: analysis by pressure-volume loops.

BACKGROUND: Acute hemodynamic effects of cardiac resynchronization therapy (CRT) were reported previously, but detailed invasive studies showing hemodynamic consequences of long-term CRT are not available. METHODS AND RESULTS: We studied 22 patients scheduled for implantation of a CRT device based on conventional criteria (New York Heart Association class III or IV, left ventricular [LV] ejection fraction <35%, left bundle-branch block, and QRS duration >120 ms). During diagnostic catheterization before CRT, we acquired pressure-volume loops using conductance catheters during atrial pacing at 80, 100, 120, and 140 bpm. Studies were repeated during biventricular pacing at the same heart rates after 6 months of CRT. Our data show a significant clinical benefit of CRT (New York Heart Association class change from 3.1+/-0.5 to 2.1+/-0.8; quality-of-life score change from 44+/-12 to 31+/-16; and 6-minute hall-walk distance increased from 260+/-149 to 396+/-129 m; all P<0.001), improved LV ejection fraction (from 29+/-10% to 40+/-13%, P<0.01), decreased end-diastolic pressure (from 18+/-8 to 13+/-6 mm Hg, P<0.05), and reverse remodeling (end-diastolic volume decreased from 257+/-67 to 205+/-54 mL, P<0.01). Previously reported acute improvements in LV function remained present at 6 months: dP/dtmax increased 18%, -dP/dtmin increased 13%, and stroke work increased 34% (all P<0.01). Effects of increased heart rate were improved toward more physiological responses for LV ejection fraction, cardiac output, and dP/dtmax. Moreover, our study showed improved ventricular-arterial coupling (69% increase, P<0.01) and improved mechanical efficiency (44% increase, P<0.01). CONCLUSIONS: Hemodynamic improvements with CRT, previously shown in acute invasive studies, are maintained chronically. In addition, ventricular-arterial coupling, mechanical efficiency, and chronotropic responses are improved after 6 months of CRT. These findings may help to explain the improved functional status and exercise tolerance in patients treated with CRT.

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PubMed2006

Effect of posterolateral scar tissue on clinical and echocardiographic improvement after cardiac resynchronization therapy.

BACKGROUND: Currently, one third of patients treated with cardiac resynchronization therapy (CRT) do not respond. Nonresponse to CRT may be explained by the presence of scar tissue in the posterolateral left ventricular (LV) segments, which may result in ineffective LV pacing and inadequate LV resynchronization. In the present study, the relationship between transmural posterolateral scar tissue and response to CRT was evaluated. METHODS AND RESULTS: Forty consecutive patients with end-stage heart failure (NYHA class III/IV), LV ejection fraction < or =35%, QRS duration >120 ms, left bundle-branch block, and chronic coronary artery disease were included. The localization and transmurality of scar tissue were evaluated with contrast-enhanced MRI. Next, LV dyssynchrony was assessed at baseline and immediately after implantation with tissue Doppler imaging. Clinical parameters, LV volumes, and LV ejection fraction were assessed at baseline and at a 6-month follow-up. Fourteen patients (35%) had a transmural (>50% of LV wall thickness) posterolateral scar. In contrast to patients without posterolateral scar tissue, these patients showed a low response rate (14% versus 81%; P<0.05) and did not show improvement in clinical or echocardiographic parameters. In addition, LV dyssynchrony remained unchanged after CRT implantation (84+/-46 versus 78+/-41 ms; P=NS). Patients without posterolateral scar tissue and severe baseline dyssynchrony (> or =65 ms) showed an excellent response rate of 95% compared with patients with a posterolateral scar and/or absent LV dyssynchrony (11%). CONCLUSIONS: CRT does not reduce LV dyssynchrony in patients with transmural scar tissue in the posterolateral LV segments, resulting in clinical and echocardiographic nonresponse to CRT.

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PubMed2006

Beneficial hemodynamic and clinical effects of surgical ventricular restoration in patients with ischemic dilated cardiomyopathy.

BACKGROUND: Surgical ventricular restoration is increasingly applied in patients with ischemic dilated cardiomyopathy. Previous studies show promising results with regard to survival and clinical outcome. However, a comprehensive midterm analysis of this approach on left ventricular (LV) and right ventricular function is not yet available. We investigated biventricular function and clinical status at 6-month follow-up. METHODS: We investigated the effects of surgical ventricular restoration on clinical variables, LV volume, right ventricular reverse remodeling, LV dyssynchrony, tricuspid regurgitation, and pulmonary artery pressure in 21 patients with ischemic dilated cardiomyopathy (New York Heart Association class III or IV) who underwent surgical ventricular restoration and coronary artery bypass grafting. Additional surgery included mitral annuloplasty (n = 14) and tricuspid valve annuloplasty (n = 8). Clinical variables (New York Heart Association class, quality-of-life questionnaire, 6-minute hall-walk test) and echocardiographic variables were assessed at baseline and at 6 months. RESULTS: At 6-month follow-up, all clinical variables were significantly improved. Left ventricular ejection fraction improved from 0.27 +/- 0.10 to 0.36 +/- 0.11 (p < 0.01), LV end-diastolic volume decreased from 248 +/- 78 mL to 152 +/- 50 mL (p < 0.001), and LV end-systolic volume decreased from 186 +/- 77 mL to 101 +/- 50 mL (p < 0.001). Left ventricular dyssynchrony decreased from 61 +/- 41 ms to 12 +/- 12 ms (p < 0.001). Right ventricular annular diameter decreased from 30 +/- 7 mm to 27 +/- 6 mm, right ventricular short-axis from 30 +/- 9 mm to 27 +/- 7 mm, and right ventricular long-axis from 90 +/- 7 mm to 79 +/- 10 mm (all p < 0.05). Finally, significant reductions in severity of tricuspid regurgitation (from 1.3 +/- 1.1 to 0.9 +/- 0.6; p = 0.001) and pulmonary artery pressure (42 +/- 11 mm Hg to 28 +/- 10 mm Hg; p = 0.015) were observed. CONCLUSIONS: Surgical ventricular restoration resulted in improvement of clinical variables, significant LV volume reduction, and reduced LV dyssynchrony at 6-month follow-up. In addition, right ventricular reverse remodeling was noted with reductions in tricuspid regurgitation and pulmonary artery pressure.

Adult↗
PubMed2006

Surgical ventricular restoration in patients with ischemic dilated cardiomyopathy: evaluation of systolic and diastolic ventricular function, wall stress, dyssynchrony, and mechanical efficiency by pressure-volume loops.

OBJECTIVES: Surgical ventricular restoration aims at improving cardiac function by normalization of left ventricular shape and size. Recent studies indicate that surgical ventricular restoration is highly effective with an excellent 5-year outcome in patients with ischemic dilated cardiomyopathy. We used pressure-volume analysis to investigate acute changes in systolic and diastolic left ventricular function, mechanical dyssynchrony and efficiency, and wall stress. METHODS: In 3 patient groups (total, n = 33), pressure-volume loops were measured by conductance catheter before and after surgery. The main study group consisted of 10 patients with ischemic dilated cardiomyopathy (New York Heart Association class III/IV, left ventricular ejection fraction <30%) who had surgical ventricular restoration and coronary artery bypass grafting. In this group, 7 patients had additional restrictive mitral annuloplasty. To assess potential confounding effects of restrictive mitral annuloplasty and cardiopulmonary bypass, we included a group of 10 patients (New York Heart Association class III/IV, left ventricular ejection fraction <30%) who had isolated restrictive mitral annuloplasty and a group of 13 patients with preserved left ventricular function who had isolated coronary artery bypass grafting. RESULTS: After surgical ventricular restoration, end-diastolic and end-systolic volumes were reduced from 211 +/- 54 to 169 +/- 34 mL (P = .03) and from 147 +/- 41 to 110 +/- 59 mL (P = .04), respectively. Left ventricular ejection fraction (from 27% +/- 7% to 37% +/- 13%, P = .04) and end-systolic elastance (from 1.12 +/- 0.71 to 1.57 +/- 0.63 mm Hg/mL, P = .03) improved. Peak wall stress (from 358 +/- 108 to 244 +/- 79 mm Hg, P < .01) and mechanical dyssynchrony (from 26% +/- 4% to 19% +/- 6%, P < .01) were reduced, whereas mechanical efficiency improved (from 0.34 +/- 13 to 0.49 +/- 0.14, P = .03). End-diastolic pressure increased (from 13 +/- 6 to 20 +/- 5 mm Hg, P < .01), whereas the diastolic chamber stiffness constant tended to be increased (from 0.021 +/- 0.009 to 0.037 +/- 0.021 mL(-1), NS). CONCLUSIONS: Surgical ventricular restoration achieves normalization of left ventricular volumes and improves systolic function and mechanical efficiency by reducing left ventricular wall stress and mechanical dyssynchrony.

Biomechanical Phenomena↗
PubMed2006

Intramyocardial injection of skeletal myoblasts: long-term follow-up with pressure-volume loops.

The human heart has a limited capacity for self-repair because, unlike most other cells, cardiomyocytes do not regenerate. Therefore, if a substantial number of myocytes is lost after a myocardial infarction, the performance of the heart may become severely limited, leading to a condition of heart failure. Recently, cell transplantation has emerged as a potential therapy for patients with end-stage heart failure. Of the various cell types being investigated for this purpose, skeletal myoblasts are an attractive option, because they are readily available from muscle biopsies and, if autologous cells are used, immunosuppression is not required and ethical issues are avoided. Several studies have shown that the cells can survive and differentiate after transplantation, and promising clinical results have been reported. However, effects of this therapy on left ventricular function remain largely unknown. In the present study, we investigated the long-term hemodynamic effects of intramyocardial injection of autologous skeletal myoblasts in patients with ischemic heart failure. Our findings indicate hemodynamic improvement after follow-up for up to 1 year, which is especially promising in view of the expected decline in left ventricular function in these patients.

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PubMed2006

Left ventricular dyssynchrony in patients with heart failure: pathophysiology, diagnosis and treatment.

The number of patients with chronic heart failure is increasing rapidly in the Western world. Despite the introduction of new pharmacologic therapies, the prognosis of these patients remains poor. Left ventricular (LV) dyssynchrony is a frequently observed feature in patients with heart failure, and is recognized as an important predictor of poor outcome if left untreated. The presence of LV dyssynchrony leads to inefficient LV contraction with a decreased cardiac output. Moreover, patients with LV dyssynchrony are at increased risk of adverse cardiac events. New therapeutic options targeted at restoring normal mechanical synchrony, such as cardiac resynchronization therapy, have been shown to improve clinical symptoms and prognosis in patients with heart failure. The beneficial effects of cardiac resynchronization therapy are predominantly mediated by this treatment's ability to reduce LV dyssynchrony. Given these results, adequate identification of LV dyssynchrony in patients with heart failure is of paramount importance. Several new imaging techniques are proving useful for diagnosis of LV dyssynchrony. In particular, advanced echocardiographic techniques (e.g. tissue Doppler imaging) and conductance catheter techniques are two accurate methods for quantification of LV dyssynchrony. In this review, we discuss the pathophysiology, diagnosis and treatment of LV dyssynchrony in patients with heart failure.

Arrhythmias, Cardiac↗
PubMed2006

The effect of lung inflation on absolute ventricular volume measurement by conductance.

BACKGROUND: Conductance catheter in vivo ventricular volume measurements during lung ventilation may provide important information on left ventricular (LV) function. Breathing potentially may alter parallel conductance (V(c)), complicating interpretation of the conductance-derived volume signals. The effects of controlled positive pressure lung inflation (PPLI) on measured parallel conductance with dual-field conductance volumetry were investigated. METHODS: Eight anaesthetized pigs were instrumented with an LV dual-field conductance volumetry catheter. V(c) was measured repeatedly, using the hypertonic saline injection method, at three different levels of lung insufflation: continuous positive airway pressure (PPLI) 0, 5, and 10 cm H(2)O. RESULTS: V(c)s measured at PPLI 0, 5 and 10 cm H(2)O were 70.9 +/- 4.8, 70.7 +/- 5.5 and 70.5 +/- 5.9 ml, respectively. The corresponding uncalibrated end-diastolic volumes (EDV(u)) were 115.5 +/- 7.1, 117.0 +/- 7.5 and 117.5 +/- 7.7 ml, respectively. Mean coefficients of variance for V(c) and EDV(u) at all three PPLI levels were 3.8% and 1.25%, respectively. DISCUSSION: Several levels of PPLI demonstrated no systematic change in parallel conductance for LV dual-field conductance volume signal. We concluded that lung inflation at these levels does not generate changes in V(c).

Animals↗
PubMed2006

Extent of viability to predict response to cardiac resynchronization therapy in ischemic heart failure patients.

UNLABELLED: The response to cardiac resynchronization therapy (CRT) varies significantly among individuals. Preliminary data suggest that the presence of myocardial viability may be important for response to CRT. The aim of this study was to evaluate whether the extent of viability could predict response to CRT after 6 mo. METHODS: Sixty-one consecutive patients with advanced heart failure, left ventricular ejection fraction < 35%, QRS duration > 120 ms, and chronic coronary artery disease were included. To determine the extent of viability all patients underwent nuclear imaging with 18F-FDG SPECT before implantation. Clinical and echocardiographic parameters were assessed at baseline and after 6 mo of follow-up. RESULTS: The presence of myocardial viability was directly related to an increase in left ventricular ejection fraction after 6 mo of CRT. Furthermore, the extent of viability in responders (n = 38) was significantly larger compared with that of nonresponders (n = 23; 12 +/- 3 vs. 7 +/- 3 viable segments, P < 0.01). Moreover, the optimal cutoff value to predict clinical response to CRT was identified at an extent of 11 viable segments or more (in a 17-segment model), yielding a sensitivity of 74% and a specificity of 87%. CONCLUSION: The presence of myocardial viability is directly related to response to CRT in patients with ischemic heart failure. Interestingly, using a cutoff level of 11 viable segments or more, the extent of viability could be used to predict response. Therefore, evaluation for myocardial viability may be considered in the selection process for CRT.

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