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Biomedical subjects

Michael H Picard

Publications and source records attributed to Michael H Picard.

At least 19 recordsLinked to original sources
PubMed2007

Infarct size assessment in mice.

Genetically modified mice are used extensively in models of ischemia reperfusion (I/R) and nonreperfused myocardial infarction (MI) to gain insights into pathways involved in these pathologies. Echocardiography is an ideal noninvasive tool to serially monitor the cardiac murine phenotype. The present review details the surgical aspects of I/R and MI models and the measurement of MI size by pathology techniques and the input of echocardiographic techniques including the extent of wall motion abnormality and of perfusion defects using myocardial contrast echocardiography in the assessment of murine area at risk and MI size.

Animals↗
PubMed2006

Cardiomyocyte-specific overexpression of nitric oxide synthase 3 prevents myocardial dysfunction in murine models of septic shock.

Myocardial dysfunction contributes to the high mortality of patients with endotoxemia. Although nitric oxide (NO) has been implicated in the pathogenesis of septic cardiovascular dysfunction, the role of myocardial NO synthase 3 (NOS3) remains incompletely defined. Here we show that mice with cardiomyocyte-specific NOS3 overexpression (NOS3TG) are protected from myocardial dysfunction and death associated with endotoxemia. Endotoxin induced more marked impairment of Ca(2+) transients and cellular contraction in wild-type than in NOS3TG cardiomyocytes, in part, because of greater total sarcoplasmic reticulum Ca(2+) load and myofilament sensitivity to Ca(2+) in the latter during endotoxemia. Endotoxin increased reactive oxygen species production in wild-type but not NOS3TG hearts, in part, because of increased xanthine oxidase activity. Inhibition of NOS by N(G)-nitro-l-arginine-methyl ester restored the ability of endotoxin to increase reactive oxygen species production and xanthine oxidase activity in NOS3TG hearts to the levels measured in endotoxin-challenged wild-type hearts. Allopurinol, a xanthine oxidase inhibitor, attenuated endotoxin-induced reactive oxygen species accumulation and myocardial dysfunction in wild-type mice. The protective effects of cardiomyocyte NOS3 on myocardial function and survival were further confirmed in a murine model of polymicrobial sepsis. These results suggest that increased myocardial NO levels attenuate endotoxin-induced reactive oxygen species production and increase total sarcoplasmic reticulum Ca(2+) load and myofilament sensitivity to Ca(2+), thereby reducing myocardial dysfunction and mortality in murine models of septic shock.

Actin Cytoskeleton↗
PubMed2006

Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon.

BACKGROUND: Multiple studies have individually documented cardiac dysfunction and biochemical evidence of cardiac injury after endurance sports; however, convincing associations between the two are lacking. We aimed to determine the associations between the observed transient cardiac dysfunction and biochemical evidence of cardiac injury in amateur participants in endurance sports and to elicit the risk factors for the observed injury and dysfunction. METHODS AND RESULTS: We screened 60 nonelite participants, before and after the 2004 and 2005 Boston Marathons, with echocardiography and serum biomarkers. Echocardiography included conventional measures as well as tissue Doppler-derived strain and strain rate imaging. Biomarkers included cardiac troponin T (cTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP). All subjects completed the race. Echocardiographic abnormalities after the race included altered diastolic filling, increased pulmonary pressures and right ventricular dimensions, and decreased right ventricular systolic function. At baseline, all had unmeasurable troponin. After the race, > 60% of participants had increased cTnT > 99th percentile of normal (> 0.01 ng/mL), whereas 40% had a cTnT level at or above the decision limit for acute myocardial necrosis (> or = 0.03 ng/mL). After the race, NT-proBNP concentrations increased from 63 (interquartile range [IQR] 21 to 81) pg/mL to 131 (IQR 82 to 193) pg/mL (P<0.001). The increase in biomarkers correlated with post-race diastolic dysfunction, increased pulmonary pressures, and right ventricular dysfunction (right ventricular mid strain, r=-0.70, P<0.001) and inversely with training mileage (r=-0.71, P<0.001). Compared with athletes training > 45 miles/wk, athletes who trained < or = 35 miles/wk demonstrated increased pulmonary pressures, right ventricular dysfunction (mid strain 16+/-5% versus 25+/-4%, P<0.001), myocyte injury (cTnT 0.09 versus < 0.01 ng/mL, P<0.001), and stress (NT-proBNP 182 versus 106 pg/mL, P<0.001). CONCLUSIONS: Completion of a marathon is associated with correlative biochemical and echocardiographic evidence of cardiac dysfunction and injury, and this risk is increased in those participants with less training.

Athletic Injuries↗
PubMed2006

Echocardiographic and angiographic correlations in patients with cardiogenic shock secondary to acute myocardial infarction.

In patients with cardiogenic shock (CS) complicating acute myocardial infarction, echocardiographic and angiographic findings are used to aid diagnosis, determine prognosis, and guide management. The purpose of this analysis from the Should we emergently revascularize Occluded Coronary arteries for Cardiogenic ShocK (SHOCK) trial is to identify relations between the angiographic and echocardiographic features of patients with CS. Such an analysis of the correlations between echocardiographic and angiographic findings in patients with CS may provide insights into the etiology and treatment of CS. In 302 randomized patients, an echocardiogram and an angiogram before revascularization were available in 127 patients. Although the median ejection fraction derived by echocardiography and left ventricular angiography was identical (30%), the positive correlation was weak (R2 = 0.209, p = 0.019). Patients with a larger number of diseased vessels had worse mitral regurgitation (MR) by echocardiography (p = 0.005). There was a significant but weak association between left ventricular angiographic MR grade and echocardiographic MR severity (R2 = 0.162, p = 0.015), but there was no association between culprit vessel and degree of MR. In conclusion, worse coronary artery disease is associated with more severe MR. Echocardiography and angiography are valuable and result in similar estimated ejection fractions in a large cohort, but there is wide variation between the techniques in patients.

Aged, 80 and over↗
PubMed2006

Left ventricular lead electrical delay predicts response to cardiac resynchronization therapy.

BACKGROUND: Intracardiac electrograms can be used to guide left ventricular (LV) lead placement during implantation of cardiac resynchronization therapy (CRT) devices. Although attempts often are made to ensure that the LV lead is positioned at a site of maximal electrical delay, information on whether this is useful in predicting the acute hemodynamic response and long-term clinical outcome to CRT is limited. OBJECTIVES: The purpose of this study was to assess the ability of intracardiac (electrogram) measurements made during LV lead placement in patients undergoing CRT for predicting acute hemodynamic response and long-term clinical outcome to CRT. METHODS: Seventy-one subjects with standard indications for CRT underwent electrogram measurements and echocardiograms performed in the acute phase of this study. The LV lead electrical delay was measured intraoperatively from the onset of the surface ECG QRS complex to the onset of the sensed electrogram on the LV lead, as a percentage of the baseline QRS interval. Echocardiographic assessment of the hemodynamic response to CRT was measured as an intra-individual percentage change in dP/dt over baseline (DeltadP/dt, derived from the mitral regurgitation Doppler profile) with CRT on and off. dP/dt was measurable in 48 subjects, and acute responders to CRT were defined as those with DeltadP/dt >or=25%. Long-term response was measured as a combined endpoint of hospitalization for heart failure and/or all cause mortality at 12 months. Time to the primary endpoint was estimated by the Kaplan-Meier method, with comparisons made using the log rank test. RESULTS: LV lead electrical delay correlated weakly with DeltadP/dt of the combined group (n = 48, r = 0.311, P = .029) but was strongly correlated with DeltadP/dt in the nonischemic subgroup (n = 20, r = 0.48, P = .027). LV lead electrical delay (%) was significantly longer in acute responders (69.6 +/- 23.9 vs 31.95 +/- 11.57, P = .002) among patients with nonischemic cardiomyopathy. A reduced LV lead electrical delay (<50% of the QRS duration) was associated with worse clinical outcome within the entire cohort (hazard ratio: 2.7, 95% confidence interval: 1.17-6.68, P = .032) as well as when stratified into ischemic and nonischemic subgroups. CONCLUSION: Measuring LV lead electrical delay is useful during CRT device implantation because it may help predict hemodynamic response and long-term clinical outcome.

Aged↗
PubMed2006

Sustained improvement in left ventricular diastolic function after alcohol septal ablation for hypertrophic obstructive cardiomyopathy.

AIMS: Impaired diastolic function is responsible for many of the clinical features of hypertrophic cardiomyopathy. In patients with hypertrophic obstructive cardiomyopathy (HOCM) whose symptoms are refractory to medical therapy, alcohol septal ablation (ASA) reduces left ventricular (LV) outflow tract gradient, with short-term improvement in LV diastolic function. Little is known about the longer term impact of ASA on diastolic function. METHODS AND RESULTS: We evaluated LV diastolic function at baseline and 1- and 2-year follow-up after successful ASA. In 30 patients (58+/-15 years, 22 men) who underwent successful ASA, New York Heart Association class was lower at 1-year follow-up compared with baseline (3.0+/-0.5 to 1.5+/-0.7; P<0.0001). LV outflow tract gradient (76+/-37 to 19+/-12; P<0.0001), interventricular septal thickness (19+/-2 to 14+/-2; P<0.0001), and left atrial volume (26+/-5 to 20+/-4; P<0.0001) were decreased. Significant improvement in E-wave deceleration time, isovolumic relaxation time, early diastolic mitral lateral annular velocity (E'), mitral inflow propagation velocity (V(p)), ratio of transmitral early LV filling velocity (E) to early diastolic Doppler tissue imaging of the mitral annulus (E/E'), and E/V(p) were observed at 1 year following successful ASA. These changes persisted in the subset cohort (n=21) for whom 2-year data were available. CONCLUSION: Successful ASA for HOCM leads to significant and sustained improvement in echocardiographic measures of diastolic function, which may contribute to improved functional status after successful ASA.

Adult↗
PubMed2006

Tissue Doppler imaging predicts left ventricular dysfunction and mortality in a murine model of cardiac injury.

AIMS: Currently available non-invasive imaging methods frequently fail to detect alterations in left ventricular (LV) function despite histological evidence of injury. Tissue Doppler imaging (TDI) can detect subtle LV dysfunction. The aim of this study was to investigate whether TDI indices can predict LV systolic dysfunction and mortality following exposure to doxorubicin (DOX) in mice. METHODS AND RESULTS: TDI-derived peak endocardial systolic velocity (V(ENDO)) and strain rate (SR), as well as M-mode and two-dimensional indices of LV systolic function, were measured serially in mice after receiving DOX as a single dose (20 mg/kg). Haemodynamic measurements were obtained invasively before and at 1, 2, 4, and 5 days after the single DOX dose. Cardiac apoptosis was measured before and at 1 day after DOX. V(ENDO) and SR decreased after 1 and 2 days, respectively, whereas changes in fractional shortening (FS) and LV ejection fraction (LVEF) were not detected before 5 days. The reduction in both V(ENDO) and SR correlated with the decrease in dP/dt(MAX), and the change in V(ENDO) correlated with the early increase in cardiac cell apoptosis. In a subsequent experiment, DOX was administered at 4 mg/kg/week for 5 weeks, and LV function was followed serially for 16 weeks. In this chronic experiment, TDI indices decreased before FS and LVEF, correlated with late LV dysfunction, and predicted DOX-induced mortality. CONCLUSION: In a murine model of DOX-induced cardiac injury, TDI detects LV dysfunction prior to alterations in conventional echocardiographic indices and predicts mortality. This study suggests that TDI may be a reliable tool to detect early subtle changes in DOX-induced cardiac dysfunction.

Animals↗
PubMed2006

Usefulness of a novel "response score" to predict hemodynamic and clinical outcome from cardiac resynchronization therapy.

Cardiac resynchronization therapy (CRT) is an important treatment for patients with congestive heart failure and ventricular dyssynchrony, but response to CRT is highly variable. We assessed whether a scoring system that encompasses a combination of patient selection and procedural variables would improve prediction of CRT response. Thirty-nine patients who underwent CRT with echocardiographic assessment of baseline contractility and left ventricular (LV) dyssynchrony, intraprocedural assessment of LV lead electrical delay, and postprocedural chest radiography were included. Baseline LV dyssynchrony was measured by Doppler tissue velocity imaging as the maximum time difference between peak systolic velocity of anterior, lateral, posterior, and septal walls. The hemodynamic effect of CRT was measured by Doppler analysis of mitral regurgitation as percent change in maximal +dP/dt (DeltadP/dt) with CRT on versus off. Acute responders to CRT were defined as Deltadp/dt >or=25%. Clinical response was measured as a combined end point of hospitalization for heart failure and all-cause mortality. A 4-point response score was generated using variables associated with DeltadP/dt and assigning 1 point for a dorsoventral LV/right ventricular interlead distance>10 cm, 1 point for a LV lead electrical delay>or=50%, 1 point for a baseline maximum +dP/dt <600 mm Hg/s, and 1 point for a maximum time difference>100 ms. In conclusion, there was a significant association between response score (0 to 4 points) and acute hemodynamic response to CRT (p<0.0001). Kaplan-Meier analysis associated a higher response score with improved 12-month event-free survival after CRT implantation (p=0.0019).

Aged↗
PubMed2006

Time course of pressure gradient response after first alcohol septal ablation for obstructive hypertrophic cardiomyopathy.

Alcohol septal ablation (ASA) causes remodeling of the upper septum and left ventricular outflow tract (LVOT) and reduction in the LVOT gradient. The time course of gradient reduction early after ASA has not been established. This study characterized the time course of gradient response early after ASA. Patients underwent clinical assessment and transthoracic echocardiography at baseline and immediately, 3 days, 3 months, and 1 year after ASA. Forty-seven patients underwent ASA. The baseline LVOT gradient was 98 +/- 48 mm Hg. Three-month echocardiographic success, defined as > or = 50% gradient reduction from baseline, was achieved in 41 procedures (87%); thus, there were 6 failures. On the basis of percentage reduction in LVOT gradient at 3 days, 2 distinct subgroups of the success group were identified. These were monophasic success (> or = 50% gradient reduction at 3 days and 3 months, n = 25) and triphasic success (< 50% gradient reduction at 3 days but > or = 50% gradient reduction at 3 months, n = 16). LVOT gradient in the triphasic success group was similar to that in the failure group at 3 days (81 +/- 28 vs 99 +/- 31 mm Hg, p = NS) but similar to that of the monophasic success group at 3 months (24 +/- 20 vs 12 +/- 16 mm Hg, p = NS) and at 1 year (27 +/- 24 vs 13 +/- 20 mm Hg, p = NS). In conclusion, many patients who undergo ultimately successful ASA demonstrate triphasic LVOT gradient response patterns, with a large gradient 3 days after the procedure.

Analysis of Variance↗
PubMed2006

Persistent and reversible cardiac dysfunction among amateur marathon runners.

AIMS: Transient systolic and diastolic abnormalities in ventricular function have previously been documented during endurance sports. However, these described alterations may be limited by the techniques applied. We sought, using less load-dependent methods, to characterize both the extent and the chronology of the cardiac changes associated with endurance events. METHODS AND RESULTS: Transthoracic echocardiography (TTE) was performed prior to, immediately after, and approximately 1 month after completion of the 2003 Boston Marathon in 20 amateur athletes. TTE included two-dimensional, spectral and tissue Doppler (TD) and flow propagation velocity (V(p)). After completion of the marathon, global measures of left ventricular (LV) systolic function were unchanged (EF 59 +/- 6 vs. 61 +/- 4% post, P = 0.14), whereas TD-derived measures of LV systolic function [septal strain -23 +/- 5 vs. -17 +/- 4%, P = 0.007; septal strain rate (SR) -1.5 +/- 0.3 vs. -1.1+/- 0.2 s(-1), P = 0.007] and right ventricular (RV) systolic function (RV apical strain -33 +/- 4 vs. -27 +/- 5%, P = 0.001; RV apical SR -2.4 +/- 0.7 vs. -1.8 +/- 0.5, P = 0.002) were reduced. Significant changes in transmitral velocity (E/A ratio 2.0 +/- 0.5 vs.1.3 +/- 0.3, P = 0.005) and TD indices of LV and RV diastolic function (E(a) septal 9.5 +/- 1.8 vs. 8.1 +/- 1.2 cm/s post-marathon, P = 0.01) were also observed, indicating an inherent alteration in LV relaxation. Although all indices of LV and RV systolic function had returned to normal on follow-up, there were persistent diastolic abnormalities (RV E(a), 11.5 +/- 1.5 cm/s pre-marathon vs. 10.0 +/- 1.6 cm/s follow-up, P = 0.01). CONCLUSION: Marathon running leads to transient systolic and more persistent diastolic dysfunction of both the LV and the RV.

Adult↗
PubMed2006

Nitric oxide synthase 2 and pressure-overload-induced left ventricular remodelling in mice.

Nitric oxide synthase 2 (NOS2) has been reported to increase in hypertrophied cardiomyocytes; however, whether NOS2 plays a role in the development of hypertrophy is unknown. To investigate the relationship of NOS2 with left ventricular (LV) remodelling and hypertrophy following prolonged pressure overload, we studied 18 male wild-type (WT) and 20 male NOS2-deficient (NOS2-/-) mice before and 7, 14 and 28 days after transverse aortic constriction (TAC) using echocardiography. A subgroup of eight WT and eight NOS2-/- mice were studied 42 days after TAC. Haemodynamic measurements were obtained before killing. Left ventricular size and function were similar for both genotypes at baseline. After TAC for 28 days, both groups developed LV hypertrophy, with echo-derived LV mass increasing from 78 +/- 2 to 147 +/- 10 mg in WT and from 86 +/- 3 to 142 +/- 10 mg in NOS2-/- mice. Twenty-eight days after TAC, LV weight and cardiomyocyte width were also similar in both genotypes. Fractional shortening (FS) decreased on day 7 from 57 +/- 1 to 48 +/- 2% in WT and from 59 +/- 1 to 49 +/- 2% in NOS2-/- mice. Although this decrease in FS was transient in WT mice, it persisted in NOS2-/- mice. Invasively measured parameters of systolic and diastolic function, however, were similar in the two genotypes both 28 and 42 days after TAC. A load-independent index of contractility, Emax, was similar in both strains 42 days after TAC. In conclusion, NOS2 does not appear to have a critical role in the development of LV hypertrophy after chronic pressure overload.

Animals↗
PubMed2006

NT-proBNP levels, echocardiographic findings, and outcomes in breathless patients: results from the ProBNP Investigation of Dyspnoea in the Emergency Department (PRIDE) echocardiographic substudy.

AIMS: The objective of this study was to determine the integrative utility of measuring plasma NT-proBNP levels with echocardiography in the evaluation of dyspnoeic patients. METHODS AND RESULTS: Of 599 emergency department patients enrolled in a clinical study of NT-proBNP at a tertiary-care hospital, 134 (22%) had echocardiographic results available for analysis. Echocardiographic parameters correlating with NT-proBNP levels were determined using multivariable linear-regression analysis. Independent predictors of 1-year mortality were determined using Cox-proportional hazard analysis. Independent relationships were found between NT-proBNP levels and ejection fraction (P = 0.012), tissue Doppler early and late mitral annular diastolic velocities (P = 0.007 and 0.018), right ventricular (RV) hypokinesis (P = 0.006), and tricuspid regurgitation severity (P < 0.001) and velocity (P = 0.007). An NT-proBNP level <300 pg/mL had a negative predictive value of 91% for significant left ventricular systolic and diastolic dysfunction. Overall 1-year mortality was 20.1% and was independently predicted by NT-proBNP level [HR 8.65, 95% confidence interval (CI) 2.7-27.8, P = 0.0003], ejection fraction (HR 0.95, 95% CI 0.91-0.99, P = 0.009), RV dilation (HR 2.98, 95% CI 1.05-12.8, P = 0.04), and systolic blood pressure (HR 0.97, 95% CI 0.96-0.99, P = 0.01). CONCLUSION: NT-proBNP levels correlate with, and provide important prognostic information beyond, echocardiographic parameters of cardiac structure and function. Routine NT-proBNP testing may thus be useful to triage patients to more timely or deferred echocardiographic evaluation.

Dyspnea↗
PubMed2006

Left ventricular function after exercise training in young men.

The effects of endurance training have been extensively studied in athletes, but longitudinal studies of exercise-induced cardiac changes in normal patients are limited. To assess the effects of 6 months of moderate-intensity aerobic training (1 hour/day, 3 times/week) on normal hearts, 23 sedentary men aged 31.1 +/- 3.5 years were studied by standard and tissue Doppler echocardiography. Left ventricular (LV) systolic function was assessed by the ejection fraction and Doppler-measured stroke volume, and diastolic function was assessed by transmitral and pulmonary venous flow. Tissue Doppler systolic (Sm), early (Em), and late (Am) myocardial velocities were obtained at the septal and lateral mitral annulus. After training, there was a 14.5% increase in peak oxygen consumption (p = 0.000002) and a decrease in heart rate (60 +/- 7 to 56 +/- 8 beats/min, p = 0.01). Septal and posterior wall thickness increased (8.7 +/- 1.0 to 9.4 +/- 1.3 mm, p = 0.002, and 8.2 +/- 0.7 to 8.8 +/- 1.1 mm, p = 0.0009, respectively), with a 15% increase in LV mass index (p = 0.0002). LV diameters, stroke volumes, and ejection fractions were unchanged. Mitral inflow showed a decrease in late-wave velocity (p = 0.00004), thus increasing the early (E)/A ratio. Septal and lateral Sm (p = 0.02) and Em velocities (p <0.05) increased after training. In conclusion, the physiologic increase in LV mass in response to regular exercise in healthy young men occurs in parallel with a decrease in atrial contribution to flow. LV function estimated by tissue Doppler is improved despite the lack of changes in standard echocardiographic indexes.

Adult↗
PubMed2006

Recommendations for chamber quantification.

Quantification of cardiac chamber size, ventricular mass and function ranks among the most clinically important and most frequently requested tasks of echocardiography. Over the last decades, echocardiographic methods and techniques have improved and expanded dramatically, due to the introduction of higher frequency transducers, harmonic imaging, fully digital machines, left-sided contrast agents, and other technological advancements. Furthermore, echocardiography due to its portability and versatility is now used in emergency rooms, operating rooms, and intensive care units. Standardization of measurements in echocardiography has been inconsistent and less successful, compared to other imaging techniques and consequently, echocardiographic measurements are sometimes perceived as less reliable. Therefore, the American Society of Echocardiography, working together with the European Association of Echocardiography, a branch of the European Society of Cardiology, has critically reviewed the literature and updated the recommendations for quantifying cardiac chambers using echocardiography. This document reviews the technical aspects on how to perform quantitative chamber measurements of morphology and function, which is a component of every complete echocardiographic examination.

Cardiac Volume↗
PubMed2006

Inhaled nitric oxide decreases infarction size and improves left ventricular function in a murine model of myocardial ischemia-reperfusion injury.

To learn whether nitric oxide (NO) inhalation can decrease myocardial ischemia-reperfusion (I/R) injury, we studied a murine model of myocardial infarction (MI). Anesthetized mice underwent left anterior descending coronary artery ligation for 30, 60, or 120 min followed by reperfusion. Mice breathed NO beginning 20 min before reperfusion and continuing thereafter for 24 h. MI size and area at risk were measured, and left ventricular (LV) function was evaluated using echocardiography and invasive hemodynamic measurements. Inhalation of 40 or 80 ppm, but not 20 ppm, NO decreased the ratio of MI size to area at risk. NO inhalation improved LV systolic function, as assessed by echocardiography 24 h after reperfusion, and systolic and diastolic function, as evaluated by hemodynamic measurements 72 h after reperfusion. Myocardial neutrophil infiltration was reduced in mice breathing NO, and neutrophil depletion prevented inhaled NO from reducing myocardial I/R injury. NO inhalation increased arterial nitrite levels but did not change myocardial cGMP levels. Breathing 40 or 80 ppm NO markedly and significantly decreased MI size and improved LV function after ischemia and reperfusion in mice. NO inhalation may represent a novel method to salvage myocardium at risk of I/R injury.

Administration, Inhalation↗
PubMed2006

Restrictive physiology in cardiogenic shock: observations from echocardiography.

BACKGROUND: Left ventricular diastolic abnormalities are associated with adverse outcome in myocardial infarction. Intra-aortic balloon pump (IABP) support is associated with improved diastolic filling. In the SHOCK trial and registry, average left ventricular ejection fraction (LVEF) was approximately 30%, higher than expected based on the classic paradigm. We hypothesized that restrictive physiology plays a role in cardiogenic shock (CS). METHODS: Echocardiograms obtained during the SHOCK trial within 24 hours of randomization were centrally interpreted. Patients with quantifiable mitral E-wave deceleration time were included (n = 64). The restrictive filling pattern was defined as deceleration time < 140 milliseconds. RESULTS: The restrictive pattern was seen in 60.9% of patients studied. Patients with this pattern had lower LVEF (31.1% vs 39.0%, P = .02) and higher wall motion score index (2.1 vs 1.8, P = .05). Patients with restriction were more likely to have IABP support during echocardiography (73.7% vs 43.5%, P = .03). There was no difference with and without restriction in demographic and hemodynamic variables or in mitral regurgitation degree or extent of coronary disease. The restrictive pattern had positive predictive value of 80% for pulmonary capillary wedge pressure > or = 20 mm Hg. Thirty-day survival was 53.9% with restriction versus 68.0% without restriction, P = .31. There was no difference in New York Heart Association class at 1 year between groups. CONCLUSIONS: The restrictive filling pattern is common in patients with CS, which may suggest that diastolic dysfunction contributes to CS pathogenesis. Patients with the restrictive pattern had lower LVEF despite IABP support. An association between the restrictive pattern and mortality was not demonstrated; power was limited by sample size.

Aged↗