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Biomedical subjects

Michael Y Henein

Publications and source records attributed to Michael Y Henein.

At least 19 recordsLinked to original sources
PubMed2006

Ventricular endocrine and mechanical function following thrombolysis for acute myocardial infarction.

OBJECTIVE: The objective of this study was to assess natriuretic peptide release following acute myocardial infarction, and its relationship with ventricular function. METHODS: A total of 44 patients with acute myocardial infarction were studied; 13 anterior, age (57+/-12 years) and 31 inferior, age (58+/-12 years). Peptide levels and left ventricular function by echocardiography were assessed at admission and on days 7 and 30 after thrombolysis. Healthy volunteers (n=21) served as controls. RESULTS: Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) levels rose from admission to day 7 (p=0.002). While ANP remained elevated at day 30 in both groups, BNP levels fell in patients with anterior myocardial infarction (p=0.03). Left ventricular fractional shortening was reduced at admission in the two groups (p=0.01) but returned towards normal in 7 days (p=0.001) in inferior myocardial infarction and in 30 days in anterior myocardial infarction (p=0.02). Left ventricular long axis amplitude was universally reduced at admission (p=0.01) and remained abnormal at day 30 (p=0.01) in both groups. At day 7, BNP and ANP levels inversely correlated with long axis amplitude of lateral wall in anterior myocardial infarction; (r=-0.7, p=0.01). BNP correlated inversely with fractional shortening in anterior myocardial infarction (r=-0.7, p=0.01) at day 30. CONCLUSION: The elevated peptide levels at 7 days post-myocardial infarction correlate with reduced mechanical activity of the adjacent noninfarcted segment. Natriuretic peptides release seem to be related to failure of compensatory hyperdynamic activity of the noninfarcted area rather than directly from the injured myocardial segments.

Atrial Natriuretic Factor↗
PubMed2006

Comparison of segmental and global markers of dyssynchrony in predicting clinical response to cardiac resynchronization.

AIMS: Cardiac resynchronization therapy (CRT) reduces inter- and intraventricular dyssynchrony and shortens total isovolumic time (t-IVT). We compared the extent to which the values of ventricular dyssynchrony and t-IVT predict clinical benefits of CRT. METHODS AND RESULTS: Ventricular dyssynchrony was assessed in 39 patients with heart failure before and 6 months after CRT. Segmental dyssynchrony was identified from time to onset and peak systolic velocity of wall motion. T-IVT (s/min) was derived as [60-(total ejection time+total filling time)]. The difference between ventricular pre-ejection periods (D-PEP) was calculated. Outcome measures were fall in New York Heart Association (NYHA) class and increase in cardiac output (CO). Following CRT, NYHA class fell in 29/39 patients, CO increased (by 1.0 L/min, P < 0.001), and intraventricular delay (Intra-VD), interventricular delay (Inter-VD), t-IVT, and D-PEP shortened (by 25 ms, 72 ms, 6 s/min, and 38 ms, P < 0.01). NYHA class and CO were unchanged with CRT in 10/39, and Intra-VD, Inter-VD, t-IVT, and D-PEP lengthened (by 43 ms, 52 ms, 7 s/min, and 35 ms, P < 0.05). Though univariate predictors of CO increment with CRT were Intra-VD, Inter-VD, t-IVT, and D-PEP, only pre-CRT values of CO (P < 0.001), t-IVT (P < 0.001), and D-PEP (P = 0.025) were independent. CONCLUSION: Global, rather than segmental, measures of ventricular dyssynchrony are powerful, independent predictors of clinical response to CRT.

Aged↗
PubMed2006

"Isolated" diastolic dysfunction in left ventricular outflow tract obstruction.

We sought to investigate the prescence of "isolated" diastolic disease, defined as reduced long-axis early diastolic velocity with normal systolic velocity, in 21 young patients with left outflow tract obstruction. Most patients had depressed systolic velocities despite normal ejection fractions. The close relations amond long-axis velocities suggest isolated diastolic disease is unlikely.

Adult↗
PubMed2006

Mechanism of cardiac output gain from cardiac resynchronization therapy in patients with coronary artery disease or idiopathic dilated cardiomyopathy.

The mechanisms underlying cardiac resynchronization therapy have consistently been studied at rest and remain ill defined. Peak stress total isovolumic time (t-IVT) is a major determinant of cardiac output (CO) in chronic heart failure. In this study, pharmacologic stress was used to assess the effects of atrioventricular (AV) delay shortening and ventricular resynchronization elements of cardiac resynchronization therapy. Thirty patients undergoing cardiac resynchronization therapy were studied <6 months after implantation. t-IVT and CO were measured during native activation (left bundle branch block), AV delay shortening (right ventricular dual-chamber pacing), and full resynchronization (atrio-biventricular pacing). Full resynchronization shortened peak stress t-IVT by 9.4 +/- 6.2 s/min (p <0.001) and increased peak stress CO by 0.9 +/- 0.4 L/min (p <0.001), with the effects in individual patients showing a large correlation (r = -0.64, p <0.001). In contrast, simple AV delay shortening did not shorten peak stress t-IVT nor increase peak stress CO, nor was CO at rest affected by full resynchronization or AV delay shortening. Of all measurements during native activation, the best predictor of gain in peak stress CO from full resynchronization was peak stress t-IVT (r = 0.75, p <0.001), with every 5 s/min increment in peak stress t-IVT during native activation predicting a 6% gain in peak stress CO. No conventional measures during native activation at rest or during stress (including QRS duration, the Tei index, tissue Doppler intraventricular delay, and t-IVT at rest) added significant additional information. In conclusion, only during stress does resynchronization consistently increase CO. Second, little of this increment in CO is achieved by AV delay shortening alone. Third, under native activation, long t-IVT during peak stress is the single best predictor of resynchronization-mediated increment in peak stress CO.

Aged↗
PubMed2006

Successful double bioprosthetic valve replacement in a 64-year-old man with carcinoid syndrome and bipolar disorder: case report.

The case is described of a 64-year-old man with bipolar disorder and severe carcinoid heart disease who required a double valve replacement. Multidisciplinary team involvement and extensive preoperative investigations resulted in a successful regimen which prevented reactivation of carcinoid syndrome and avoided the serious side effects of lantreotide and lithium therapy. In addition, two bioprosthetic valves were used, thereby avoiding the potential complications of anticoagulation in a patient with known hepatic metastases.

Bioprosthesis↗
PubMed2005

Doppler echocardiographic profile and indexes in the evaluation of aortic coarctation in patients before and after stenting.

OBJECTIVES: We sought to assess the effect of successful stenting on the Doppler profile of aortic coarctation and to identify echocardiographic indexes that could be used for follow-up of such patients. BACKGROUND: Doppler echocardiography demonstrates characteristic flow patterns in significant aortic coarctation. METHODS: We undertook retrospective echocardiographic analyses before and at six to nine months after coarctation stenting in consecutive patients from 2002 to 2003. Peak systolic pressure gradient (SPG), diastolic velocity (DV), end-diastolic tail velocity (EDTV), systolic velocity half-time index (SVHTi) and diastolic velocity half-time index (DVHTi), and systolic pressure half-time index (SPHTi) and diastolic pressure half-time index (DPHTi) were measured. The severity of aortic coarctation was compared with cardiovascular magnetic resonance (CMR) imaging using the coarctation index (CoAi). RESULTS: The patient cohort was divided into two groups: group 1 (13 patients; age 30 +/- 8 years), which consisted of patients with significant aortic coarctation treated with stenting, and group 2 (11 patients; age 39 +/- 16 years), which consisted of patients with previous surgical repair of aortic coarctation without evidence of re-coarctation. After stenting, there was significant reduction in SPG (p = 0.001), DV (p = 0.001), EDTV (p = 0.005), DVHTi (p = 0.001), and DPHTi (p = 0.001) values. In the patient group as a whole, there was a significant correlation between SPG and DV (r = 0.86; p < 0.001), EDTV (r = 0.80; p < 0.001), DVHTi (r = 0.56; p < 0.001), and DPHTi (r = 0.50; p = 0.002). In addition, DV >193 cm/s (100% sensitivity, 100% specificity) and diastolic/systolic velocity ratio >0.53 (100% sensitivity, 96% specificity) had high predictive values for severe aortic coarctation (CoAi <0.25). CONCLUSIONS: After stenting, peak SPG, DV, and pressure half-time indexes (i.e., DVHTi and DPHTi) decreased significantly. These findings can confidently be used in the follow-up of coarctation patients after stenting, particularly in those with limited two-dimensional images.

Adult↗
PubMed2005

Dobutamine stress-induced ischemic right ventricular dysfunction and its relation to cardiac output in patients with three-vessel coronary artery disease with angina-like symptoms.

We investigated markers of ischemic dysfunction and their relation to overall right ventricular (RV) performance during dobutamine stress echocardiography in patients who had coronary artery disease. Thirty-three patients (58 +/- 10 years old) who had 3-vessel coronary artery disease were compared with 17 age-matched controls (58 +/- 11 years old). RV long-axis amplitude (M mode), systolic and diastolic myocardial tissue Doppler velocities, and filling and ejection velocities were measured, and cardiac output (CO) was calculated at rest and during peak stress. There was no difference in RV size (inlet dimension <3.5 cm), RV systolic long-axis amplitude, systolic and diastolic velocities, peak early/late diastolic velocity ratio, and RV CO between patients and controls at rest. During stress, RV systolic long-axis amplitude increased in controls (from 24 +/- 6 to 30 +/- 5 mm) and CO increased significantly (from 4.9 +/- 1.2 to 12.5 +/- 2.1 L/min, p <0.001 for the 2 items). In contrast, RV amplitude did not change with stress in patients (from 24 +/- 5 to 22 +/- 6 mm, p = NS), and the stress-increment in CO was augmented (from 4.2 +/- 1.2 to 8.3 +/- 2.0 L/min, p <0.001 vs control stress increment). Failure to increase RV systolic amplitude >2 mm was 79% sensitive and 88% specific for detecting ischemic RV dysfunction, and there was a close correlation between stress-induced change in RV systolic amplitude and change in CO in patients (r = 0.56, p <0.001). Early diastolic velocity increased in controls (from 10.8 +/- 3.2 to 13.1 +/- 3.6 cm/s, p <0.01) but did not change in patients (from 11.5 +/- 3.7 to 11.3 +/- 4.8 cm/s, p = NS). RV shortening after ejection did not appear in any control subject but did develop in 8 of 33 patients, thus contributing to the decrease in RV peak early/late diastolic velocity ratio in patients (from 1.1 +/- 0.3 to 0.76 +/- 0.4, p <0.001) compared with that in controls (1.3 +/- 0.3 to 1.0 +/- 0.2, p <0.001). In conclusion, markers of RV dysfunction are not related to left ventricular wall motion score index or long-axis changes with stress.

Cardiac Output↗
PubMed2005

Effect of dobutamine stress on left ventricular filling in ischemic dilated cardiomyopathy: pathophysiology and prognostic implications.

OBJECTIVES: The purpose of this research was to study the effect of dobutamine on left ventricular (LV) filling in ischemic cardiomyopathy (ICM) and to determine whether restrictive filling pattern (RFP) at peak stress has prognostic value. BACKGROUND: The prognostic value of RFP at peak stress in ICM is unknown. METHODS: A total of 69 patients with ICM were studied by Doppler echocardiography at rest and stress; RFP was defined as transmitral E:A ratio > or =1.0, isovolumic relaxation time (IVRT) <80 ms, and E-wave deceleration time (EDT) <120 ms. RESULTS: A total of 42 of 69 had RFP at rest, which reverted to non-RFP at stress in 24 (EA), but persisted in 18 (EE); 27 of 69 had non-RFP at rest and peak stress (AA). In EA, IVRT and EDT lengthened (by 43 ms and 46 ms), and tricuspid regurgitation (TR) decreased (by 26 mm Hg, p < 0.01), suggesting a fall in left atrial (LA) pressure. The stress response in AA was similar to EA. In EE, IVRT and EDT shortened (by 21 ms) and TR increased (by 13 mm Hg, p < 0.01), suggesting a rise in LA pressure. Peak aortic acceleration (LV inotropy) increased by 0.8 g in EA but only by 0.2 g in EE (difference p < 0.001). Median follow-up (interquartile range) was 34 (20 to 57) months. Three-year survival for EE, EA, and AA was 49%, 79%, and 89%, respectively (p < 0.001). Compared with AA, the hazard ratio for EE was 9.5 (p < 0.001) and for EA was 1.9 (p = 0.30). CONCLUSIONS: In ischemic cardiomyopathy, persistence of restrictive filling during stress implies a striking rise in LA pressure, greatly attenuated LV inotropic response, and markedly reduced survival. Stress echocardiography uniquely identifies these high-risk patients.

Aged↗
PubMed2005

Opposite effects of coronary artery disease and hypertrophic cardiomyopathy on left ventricular long axis function during dobutamine stress.

BACKGROUND: The mechanism for reduced early diastolic long axis lengthening velocity in hypertrophic cardiomyopathy (HCM) is not known. METHODS: We measured simultaneous septal long axis amplitude and early lengthening velocity in 23 patients with HCM, 23 normal subjects and 22 patients with coronary artery disease (CAD) of left anterior descending artery. RESULTS: Resting amplitude and lengthening velocity were reduced in HCM 0.9+/-0.2 cm, 3.5+/-1.9 cm/s but equally in CAD 1.0+/-0.3 cm, 4.1+/-2.5 cm/s vs. 1.3+/-0.2 cm, 6.3+/-1.7 cm/s in normals, p < 0.01 for both vs. normal. With dobutamine stress, lengthening velocity increased by 2.7+/-1.9 cm/s (p < 0.001) in normals, by 2.8+/-2.5 cm/s (p < 0.001) in HCM but not in patients with CAD 0.5+/-2.1, p = NS. Increment in total long axis amplitude was subnormal in CAD and HCM. However, increment in lengthening velocity was higher with stress for corresponding change in amplitude in HCM compared with CAD (chi2) = 16.5, p < 0.001). An increase in early lengthening velocity by 2 cm/s was 77% sensitive and 70% specific in discriminating between HCM and CAD. Post-ejection shortening developed or worsened in all CAD patients indicating ischemia but not in any with HCM. CONCLUSIONS: Reduced peak early lengthening velocity is not specific for HCM but also occurs in CAD. Unlike CAD, lengthening velocity increases in HCM with stress and there is no aggravation of post-ejection shortening, suggesting that the abnormal relaxation is not due to subendocardial ischemia in HCM. The greater recoil velocity per unit deformation in HCM compared with CAD, indicates elastic mechanism with increased passive muscle stiffness due to fibrosis or fibre disarray.

Cardiomyopathy, Hypertrophic↗
PubMed2005

Chronic heart failure patients with restrictive LV filling pattern have significantly less benefit from cardiac resynchronization therapy than patients with late LV filling pattern.

BACKGROUND: Cardiac resynchronization fails to improve symptoms in up to one third of patients meeting criteria for this treatment, for reasons which are unclear. Indeed, the very mechanism of benefit from resynchronization is controversial. Resynchronization may work by improving ventricular filling: we tested the hypothesis that benefit from resynchronization depends on filling pattern. METHODS AND RESULTS: We assessed symptoms (NYHA class) and LV filling of 40 patients with chronic heart failure and prolonged QRS who underwent resynchronization. Fifteen had restrictive filling pattern (E velocity>or=1.0 m/s, E/A ratio>1 and E wave deceleration time<or=140 ms) and 25 had late filling pattern (single isolated A wave or summation wave filling in late diastole). At 6 months, the patients with restrictive filling failed to show the improvements observed in those with late filling. They failed to reduce NYHA class (DeltaNYHA: 27% improved one class, 66% unchanged, 7% worsened one class, P=NS; vs. 8% improved two classes, 72% improved one class and 20% unchanged, P<0.001; difference between groups, P<0.001). They failed to reduce LV end-diastolic dimension (DeltaLVEDD -0.04 cm, P=NS; vs. -0.6, P<0.001; difference between groups, P<0.05) or end-systolic dimension (DeltaLVESD -0.01 cm, P=NS; vs. -0.6, P<0.001; difference between groups, P<0.05). They failed to improve cardiac cycle efficiency (Deltatotal isovolumic [wasted] time 2.1 s/min, P=NS; vs. -5.4 s/min; difference between groups, P<0.001). CONCLUSION: Among patients routinely eligible for resynchronization, those with restrictive filling may show significantly less (and possibly no) improvement in symptom class and ventricular dimensions after resynchronization. Their failure to improve cardiac cycle efficiency may account for their attenuated clinical benefit.

Aged↗
PubMed2005

Comparison of ventricular long-axis function in patients with cardiac amyloidosis versus idiopathic restrictive cardiomyopathy.

To investigate ventricular long-axis function in cardiac amyloidosis (CA) and idiopathic restrictive cardiomyopathy (IRC), 16 patients with CA and 14 with IRC were studied. Left ventricular (LV) long-axis function was depressed in all patients with CA compared with only 36% of patients with IRC. Impairment in longitudinal function was clearly evident, even if fractional shortening and LV filling were normal. Ventricular long-axis function may be used as a sensitive marker of early systolic dysfunction. CA and IRC have quite distinct pathophysiologic profiles, raising some concerns about the appropriateness of considering them as 2 subtypes of a single nosographic entity.

Amyloidosis↗
PubMed2005

The coronary sinus conduit function: anatomical study (relationship to adjacent structures).

BACKGROUND: The mitral valve annulus (MVA) is anchored antero-medially to the aorta. Dilatation of the MVA primarily affects its postero-lateral aspect, which is related to the coronary sinus (CS). The CS and its tributaries have been used for pacing the left ventricle in patients with intractable heart failure. The aim of this study was to determine anatomical relations between the CS and its adjacent structures in 40 adult normal cadaveric heart specimens. METHODS: In 32 specimens, longitudinal sections were made along the free circumference of the MVA in 6 separate regions, 36 degrees between each, with the 0 degree marked by a line joining the centre of the CS ostium and that of the MV. In each section, the relations of the CS to the circumflex artery and the MVA were determined. CS diameter and its distance from the endocardium, just below the MVA, were also measured by a digital calliper. RESULTS: The great cardiac vein (GCV) diameter is 5.6 +/- 1.6 mm. As it leaves the interventricular groove, it curves to the left forming the base of the triangle of "Brocq and Mouchet" with the two branches of the left coronary artery, having a triple relationship with the circumflex artery. It then continues as the CS (diameter 9.3 +/- 5.3 mm) in the inferior atrioventricular groove. The end part of the GCV crosses superficial to the left circumflex artery at the level of the left marginal vein. The shortest distance between the wall of the CS and the endocardium adjacent to the MVA at the level of the anterolateral commissure is 5.2 +/- 1.6 mm, i.e. beyond the Vieussens valve. Thus, together with the CS the great cardiac vein, form a semicircular venous channel at the postero-lateral aspect of the MVA. In 37/40 hearts, this venous channel arches upwards in its middle part to be in direct contact with the left atrium. CONCLUSION: This study demonstrates an intimate proximity between the coronary sinus, at its beginning and end, and the mitral valve annulus. It also highlights the close relationship between the great cardiac vein, the annulus and the left ventricular free wall. Assessing the same relationship using the currently available imaging techniques should aid in the successful cannulation of the coronary sinus for various cardiological interventions.

Adult↗
PubMed2004

Limitation of exercise tolerance in chronic heart failure: distinct effects of left bundle-branch block and coronary artery disease.

OBJECTIVES: The aim of this study was to identify resting measurements of left ventricular (LV) function that predict exercise capacity in dilated cardiomyopathy (DCM); in particular, the effects of left bundle branch block (LBBB), coronary artery disease (CAD), and total isovolumic time (t-IVT). BACKGROUND: The t-IVT is a major determinant of cardiac output during dobutamine stress in DCM, and is itself determined by the presence or absence of LBBB and CAD. METHODS: A total of 111 patients with DCM, 51 with CAD (29 LBBB), and 60 without CAD (30 LBBB) were studied with echocardiography and cardiopulmonary exercise testing. The t-IVT (in s/min) was measured by Doppler echocardiography, and maximal oxygen consumption (peak Vo(2)) and percentage of the normal predicted peak Vo(2) (%predicted peak Vo(2)) were obtained from exercise testing. RESULTS: Left bundle branch block reduced peak Vo(2) (by 10.5 ml.kg(-1)min(-1)) and %predicted peak Vo(2) (by 33%, both p < 0.001) compared with patients without LBBB. Coronary artery disease reduced peak Vo(2) (by 5.5 ml.kg(-1)min(-1), p < 0.001) and %predicted peak Vo(2) (by 14%, p < 0.01) compared with those without CAD (p < 0.01). The t-IVT, CAD, LBBB, and QRS duration were univariate predictors of exercise tolerance, but only t-IVT and CAD were independent predictors. The t-IVT at rest correlated with peak Vo(2) (r = -0.68) and %predicted peak Vo(2) (r = -0.74, both p < 0.001). The combination of t-IVT and CAD explained 57% (r = 0.75, p < 0.001) of the total variance in exercise capacity. CONCLUSIONS: Resting t-IVT and less prominently, CAD, are major determinants of exercise tolerance in DCM. Left bundle branch block significantly determines resting t-IVT and thus peak Vo(2). Prediction of maximum exercise capacity in DCM is therefore possible from time-domain analysis of LV function at rest.

Adrenergic beta-Antagonists↗