Lower Midwall Shortening Research Articles

Preoperative risk factors associated with left ventricular dysfunction after bariatric surgery

A large proportion of patients with severe obesity remain with left ventricular (LV) dysfunction after bariatric surgery. We assessed whether preoperative evaluation by echocardiography and inflammatory proteins can identify this high-risk group. In the Bariatric Surgery on the West Coast of Norway study, 75 patients (44 ± 10 years, body mass index [BMI] 41.5 ± 4.7 kg/m2) were prospectively evaluated by echocardiography and inflammatory proteins (high-sensitivity C-reactive protein [hsCRP], serum amyloid A [SAA] and calprotectin) before and one year after Roux-en-Y gastric bypass surgery. LV mechanics was assessed by the midwall shortening (MWS) and global longitudinal strain (GLS). Bariatric surgery improved BMI and GLS, and lowered hsCRP, calprotectin and SAA (p < 0.05). MWS remained unchanged and 35% of patients had impaired MWS at 1-year follow-up. A preoperative risk index including sex, hypertension, ejection fraction (EF) and high hsCRP (index 1) or SAA (index 2) predicted low 1-year MWS with 81% sensitivity/71% specificity (index 1), and 77% sensitivity/77% specificity (index 2) in ROC analyses (AUC 0.80 and 0.79, p < 0.001). Among individuals with severe obesity, women and patients with hypertension, increased serum levels of inflammatory proteins and reduced EF are at high risk of impaired LV midwall mechanics 1 year after bariatric surgery.ClinicalTrials.gov identifier NCT01533142 February 15, 2012.

Increased inflammatory proteins in patients with severe obesity is associated with persistent myocardial dysfunction one year after bariatric surgery. The FatWest study

Abstract Background Over half of patients with severe obesity have subclinical cardiac dysfunction and about 40% maintain impaired left ventricular (LV) mechanics one year after bariatric surgery despite impressive weight reduction. Purpose To investigate whether measurement of serum markers of chronic inflammation before bariatric surgery can help identify patients with persistent postoperative cardiac dysfunction. Methods In the prospective FatWest (Bariatric Surgery on the West Coast of Norway) study 75 patients with severe obesity (44±9 years, 72% women, body mass index [BMI] 41.5±4.7 kg/m², 56% with hypertension) underwent echocardiography before and 1 year after Roux-en-Y gastric bypass surgery. We assessed LV mechanics in the radial and longitudinal direction by the midwall shortening (MWS) and global longitudinal strain (GLS). Myocardial oxygen (O2) demand was derived from the LV mass-wall stress-heart rate product. Inflammation was assessed by high-sensitive C-reactive protein, serum amyloid A and calprotectin in biobank samples. Results Preoperatively, patients with low MWS (45% of the group) had increased high-sensitive C-reactive protein, total calprotectin, and several amyloid A isoforms, and patients with high myocardial O2 demand (20%) had high total calprotectin (all p&amp;lt;0.05). In the whole study population, bariatric surgery induced a significant improvement in both BMI (12.6±3.7 kg/m²), GLS (4.74±5.20%), myocardial O2 demand and inflammatory proteins (Figure A, all p&amp;lt;0.001). However, there were no significant improvement in MWS, and 33% of patients still had low MWS at the 1-year control. In logistic regression analyses, after adjustment for sex, BMI and hypertension, increased preoperative serum total calprotectin was independently associated with high myocardial O2 demand both pre- and postoperatively (Nagelkerke R² 0.47 and 0.51, p&amp;lt;0.05). In similar analyses, higher preoperative serum total amyloid A was related to low MWS and high myocardial O2 demand 1 year after surgery (Nagelkerke R² 0.55 and 0.51, p&amp;lt;0.05). A simple preoperative risk score based on sex, hypertension, biplane ejection fraction, and serum total amyloid A above 4.0 mg/ml predicted low 1-year MWS with 79% sensitivity and 75% specificity at a value of 1.75 in Receiver Operating Characteristic (ROC) analysis (AUC 0.80, p&amp;lt;0.001) (Figure B). Low GLS was not predicted by inflammatory biomarkers at any timepoint. Conclusion Increased serum concentration of inflammatory proteins in patients with severe obesity is linked to persistently elevated myocardial O2 demand and impaired LV midwall mechanics 1 year after bariatric surgery.Figure AFigure B

Persistent cardiac organ damage in surgically and medically treated primary aldosteronism.

We compared persistent cardiac organ damage in patients treated surgically or medically for primary aldosteronism. Eighty-four patients (age 57 ± 11 years, 27% women) with primary aldosteronism underwent echocardiography at time of diagnosis and after one year of treatment (49% adrenalectomy, 51% medical treatment). Persistent cardiac organ damage was defined as presence of left ventricle (LV) hypertrophy, low LV midwall shortening, global longitudinal strain and/or enlarged left atrium both at baseline and at follow-up. At one year, a significant regression of LV hypertrophy was observed in surgically (44 vs. 22%, P = 0.039), but not in medically treated patients (60 vs. 51%, P = 0.206). The prevalence of enlarged left atrium was reduced in both groups (both P < 0.001), whereas systolic myocardial function remained unchanged. In multivariable logistic regression analysis, medical treatment [odds ratio (OR) 4.88 (95% confidence interval (CI) 1.26-18.88)] was a strong predictor of persistent LV hypertrophy independent of higher BMI [OR 1.20 (95% CI 1.04-1.38)] and presence of diabetes [OR 6.48 (95% CI 1.20-34.83), all P < 0.05]. Persistently low midwall shortening was associated with suppressed plasma renin after one year [OR 6.11 (95% CI 1.39-26.7)] and lower renal function [OR 0.96 (95% CI 0.94-0.99), both P < 0.05]. The strongest predictor of persistently low global longitudinal strain was higher HbA1c [OR 2.37 (95% CI 1.12-5.02), P = 0.024]. Persistent cardiac organ damage was more common in the medical treatment group and associated with incomplete aldosterone blockade, impaired renal function and presence of metabolic comorbidities.

Incomplete functional reverse remodelling of the left ventricle one year after bariatric surgery. Insights from the prospective FatWest study

Abstract Background Patients with severe obesity are predisposed to development of left ventricular (LV) hypertrophy with subsequent increased myocardial oxygen demand and impaired myocardial function. Bariatric surgery leads to rapid weight loss and improves cardiovascular risk profile. Purpose To assess whether LV systolic function, wall mechanics, and cardiac power improve 1 year after bariatric surgery. Methods 91 severely obese patients (43±10 years, 70% women, body mass index [BMI] 41.7±4.9 kg/m2, 55% with hypertension, 17% with diabetes mellitus) underwent echocardiography before, 6 and 14 months after Roux-en-Y gastric bypass surgery in the prospective FatWest (Bariatric Surgery on the West Coast of Norway) study. We assessed LV systolic function by biplane ejection fraction (EF), LV wall mechanics by midwall shortening (MWS) and global longitudinal strain (GLS), and cardiac power normalized for LV mass by 0.222 x cardiac output x mean blood pressure (BP)/LV mass. Results Surgery induced a significant reduction in BMI, heart rate, systolic BP, and LV mass (Figure 1). Prevalence of LV hypertrophy fell from 34 to 20% 14 months after surgery (p&amp;lt;0.001), while that of concentric geometry remained stable: 8 vs 10% (p=0.36). GLS improved by 28%, however LV EF and MWS did not change (Figure 2). LV power at rest decreased postoperatively, reflecting the lower BP and heart rate, but was unaltered when normalized for LV mass (Figure 2). In backward stepwise multivariate regression analyses, 1 year improvement in GLS was predicted by the systolic BP reduction (p&amp;lt;0.05) (R2 0.73, p&amp;lt;0.001), while low 1-year MWS was independently associated with female gender, concentric geometry and higher myocardial oxygen demand (all p&amp;lt;0.01) (Nagelkerke R2 0.44, p&amp;lt;0.001), and lower 1-year LV power-mass with female gender and LV hypertrophy (p&amp;lt;0.01) (R2 0.24, p&amp;lt;0.001). Conclusion In severely obese patients, LV longitudinal function normalizes 1 year after bariatric surgery, mainly due to the BP reduction. LV midwall mechanics and power do not improve, especially in women and patients with persistent LV geometric abnormalities. Funding Acknowledgement Type of funding sources: None. Figure 1Figure 2

Abstract P142: Factors Associated With Persistent Cardiac Organ Damage In Primary Aldosteronism After One Year Of Treatment

Introduction: Adrenalectomy and medical treatment of primary aldosteronism (PA) both induce regression of left ventricle (LV) hypertrophy, while the effects on LV myocardial function are less investigated. Hypothesis: We hypothesized that persistent cardiac organ damage was more prevalent in medically treated PA patients. Methods: Eighty-four patients (57±11 years, 27% female) with PA underwent echocardiography at time of diagnosis and after 1 year of treatment (49% adrenalectomized, 51% medically treated). Persistent cardiac organ damage was identified as LV hypertrophy or low LV systolic function by midwall shortening or global longitudinal strain (GLS), both at baseline and at follow-up. LV diastolic function was assessed by left atrial enlargement and estimated LV filling pressure (E/e’). Results from logistic regression analyses are reported as odds ratio (OR) with 95% confidence intervals (CI). Results: After 1 year, a significant regression of LV hypertrophy was observed in adrenalectomized patients (44% vs. 22%, p=0.038), but not in medically treated patients (59% vs. 50%, p=0.206). Midwall shortening, E/e’ and prevalence of enlarged left atrium improved significantly in both treatment groups (all p&lt;0.001), while GLS remained unchanged. In multivariable logistic regression analysis, receiving medical treatment for PA (OR 4.98 [95% CI 1.26-18.88] was a strong predictor of persistent LV hypertrophy independent of higher body mass index (OR 1.20 [95% CI 1.04-1.38]) and presence of diabetes (OR 6.48 [95% CI 1.20-34.83], all p&lt;0.05). Important covariables of persistently low midwall shortening were persistent LV hypertrophy (OR 3.50 [95% CI 1.12-10.96]) and suppression of plasma renin activity after 1 year of treatment (OR 4.31 [1.15-16.12], both p&lt;0.05). The strongest predictor of persistently low GLS was higher HbA 1c (OR 2.37[95% CI 1.12-5.02], p=0.024). Conclusions: In PA, LV hypertrophy regression was more common in adrenalectomized patients. Persistent LV hypertrophy and impaired glucose metabolism were the major factors associated with persistent LV myocardial dysfunction independent of treatment.

One-year impact of bariatric surgery on left ventricular mechanics: results from the prospective FatWest study.

AimsPatients with severe obesity are predisposed to left ventricular (LV) hypertrophy, increased myocardial oxygen demand, and impaired myocardial mechanics. Bariatric surgery leads to rapid weight loss and improves cardiovascular risk profile. The present prospective study assesses whether LV wall mechanics improve 1 year after bariatric surgery.Methods and resultsNinety-four severely obese patients [43 ± 10 years, 71% women, body mass index (BMI) 41.8 ± 4.9 kg/m2, 57% with hypertension] underwent echocardiography before, 6 months and 1 year after gastric bypass surgery in the FatWest (Bariatric Surgery on the West Coast of Norway) study. We assessed LV mechanics by midwall shortening (MWS) and global longitudinal strain (GLS), LV power/mass as 0.222 × cardiac output × mean blood pressure (BP)/LV mass, and myocardial oxygen demand as the LV mass-wall stress-heart rate product. Surgery induced a significant reduction in BMI, heart rate, and BP (P < 0.001). Prevalence of LV hypertrophy fell from 35% to 19% 1 year after surgery (P < 0.001). The absolute value of GLS improved by—4.6% (i.e. 29% increase in GLS) while LV ejection fraction, MWS, and LV power/mass remained unchanged. In multivariate regression analyses, 1 year improvement in GLS was predicted by lower preoperative GLS, larger mean BP, and BMI reduction (all P < 0.05). Low 1-year MWS was associated with female sex, preoperative hypertension, and higher 1-year LV relative wall thickness and myocardial oxygen demand (all P < 0.001).ConclusionIn severely obese patients, LV longitudinal function is largely recovered one year after bariatric surgery due to reduced afterload. LV midwall mechanics does not improve, particularly in women and patients with persistent LV geometric abnormalities.ClinicalTrials.gov identifierNCT01533142, 15 February 2012.

Abstract 16319: Large Weight Loss Improves Left Ventricular Geometry but Not Myocardial Function 6 Months After Bariatric Surgery (the Fatwest Study)

Background: Bariatric surgery causes rapid and large weight loss and improves cardiovascular risk profile, yet the effect on left ventricular (LV) systolic function has been less explored. Methods: In the prospective FatWest (Bariatric Surgery on the West Coast of Norway) study 98 severely obese patients (44±10 years, 72% women, preoperative body mass index [BMI] 41.8±4.8 kg/m 2 , 36% with hypertension) underwent echocardiography before and 5.9 months after gastric bypass surgery. We assessed changes in LV geometry and systolic function by biplane ejection fraction (EF), midwall shortening (MWS) and mitral annular systolic velocity (s′). LV hypertrophy was defined based on LV mass/height 2.7 . Myocardial O 2 demand was derived from the LV mass-wall stress-heart rate product. Results: Patients experienced on average a 10 kg/m 2 reduction in BMI, and a significant drop in heart rate and blood pressure (all p&lt;0.001). LV mass (-12 g) and myocardial O 2 demand improved significantly (all p&lt;0.01). However, LV EF (60 vs. 61%), s’ (8.5 vs. 8.3cm/s) and MWS (16.1 vs. 15.7%) remained unchanged, and 45% of patients had low MWS 6 months after surgery (Figure). In multivariable regression analyses, LV mass reduction was predicted by weight loss and female sex, independent of changes in blood pressure and heart rate (R 2 0.24, p &lt;0.001) while lower myocardial O2 demand was explained by improvement in its three components, particularly lower LV end-systolic wall stress (R 2 0.9, p&lt;0.001). Conclusion: In severely obese patients with normal EF, bariatric surgery induces a significant reduction in BMI, LV mass and myocardial O 2 demand, but no improvement in LV myocardial systolic function 6 months after surgery.

Left ventricular myocardial oxygen demand and subclinical dysfunction in patients with severe obesity referred for bariatric surgery

Background and aimsIncreased myocardial oxygen (O2) demand carries higher cardiovascular risk in hypertension. We hypothesized that myocardial O2 demand is increased in severe obesity and linked to early left ventricular (LV) dysfunction. Methods and resultsBaseline data from 106 severely obese subjects referred for gastric bypass surgery (42 ± 11 years, 74% women, body mass index [BMI] 41.9 ± 4.8 kg/m2, 32% with hypertension) in the prospective FatWest (Bariatric Surgery on the West Coast of Norway) study was used. LV systolic function was assessed by biplane ejection fraction (EF), midwall shortening (MWS) and endocardial global longitudinal strain (GLS), and LV diastolic function by mitral annular early diastolic velocity (e’). Myocardial O2 demand was estimated from the LV mass-wall stress-heart rate product (high if > 1.62 × 106/2.29 × 106 g kdyne/cm2 bpm in women/men). High myocardial O2 demand was found in 33% and associated with higher BMI and high prevalence of low GLS (65%) and low MWS (63%) despite normal EF. In ROC analyses, higher myocardial O2 demand discriminated between patients with low vs. normal MWS and GLS (area under curve 0.71 and 0.63, p < 0.05). In successive multiple regression analyses, higher myocardial O2 demand was associated with lower LV MWS, GLS and average e’, respectively, independent of age, gender, BMI, pulse pressure, diabetes mellitus, and EF (all p < 0.05). ConclusionIn obese patients without known heart disease and with normal EF referred for bariatric surgery, high myocardial O2 demand is associated with lower myocardial function whether assessed by GLS or MWS independent of confounders. Clinicaltrials.gov identifierNCT01533142;

Concomitant hypertension is associated with abnormal left ventricular geometry and lower systolic myocardial function in overweight participants: the FAT associated CardiOvasculaR dysfunction study.

We studied the impact of concomitant hypertension on left ventricular (LV) systolic myocardial function and geometry in apparently healthy women and men with increased BMI. We performed a cross-sectional analysis of 535 participants (59% women) with BMI greater than 27 kg/m without known cardiovascular disease enrolled in the FAT associated CardiOvasculaR dysfunction (FATCOR) study. Hypertension was defined as use of antihypertensive treatment or elevated 24-h ambulatory blood pressure. Abnormal LV geometry was identified as increased relative wall thickness and/or LV mass index. Systolic myocardial function was assessed by midwall shortening (MWS) and speckle tracking peak global longitudinal strain (GLS). Hypertensive participants were older (49 vs. 46 years), had higher BMI and waist circumference, higher prevalences of diabetes and abnormal LV geometry (29 vs. 16%), and lower GLS (-19 vs. -20%) and MWS (16.3 vs. 17.1%) compared with normotensive participants (all P < 0.01). In multivariable linear regression analyses, hypertension was associated with lower GLS (β=0.11, P = 0.035) and lower MWS (β=0.09, P = 0.029) independent of sex, diabetes, LV hypertrophy, ejection fraction, and waist circumference. Hypertension was also associated with presence of abnormal LV geometry [odds ratio 1.74 (95% confidence interval 1.04-2.89), P = 0.035) independent of the same confounders. When replacing waist circumference with BMI in the models, hypertension retained its association with lower myocardial function, whereas the association with abnormal LV geometry was attenuated. In participants with increased BMI without known clinical cardiovascular disease, concomitant hypertension was associated with lower systolic myocardial function and more abnormal LV geometry. URL: http://www.clinicaltrials.gov NCT02805478.

Sensitivity, specificity, and accuracy of left ventricular systolic function indices and structure in detecting early systolic dysfunction assessed by speckle-tracking two-dimensional strain: An echocardiographic cross-sectional study

Background: Reduced global longitudinal strain (GLS) is an early marker of subclinical left ventricular (LV) dysfunction, permitting timely interventions to slow disease progression. This technique is not widely available in echocardiographs in routine use. Aim: We sought to know if LV systolic function indices and structural left heart changes could predict a reduced GLS. Methods: We carried out a cross-sectional analytic study in May 2017. We measured GLS (reference test), LV ejection fraction, LV midwall shortening (MWS), LV mass index, LV diastolic diameter, LV volumes, and left atrial volume (predictors). We calculated the sensitivity, specificity, accuracy, predictive values, and likelihood ratios of the predictor variables. We assessed the discriminatory power of the indices with the Youden Index and area under the receiver operator characteristic curve (AUC). Results: A total of 32 participants (14 males) were retained for this study. Their mean (standard deviation) age was 62 (15.3) years. Eccentric LV hypertrophy (LVH) was the most frequent LV geometric pattern – 14 (43.8%) participants. A reduced GLS was the most frequent LV functional anomaly – 20 (62.5%) participants. A low MWS

Low-Flow Aortic Stenosis in Asymptomatic Patients: Valvular–Arterial Impedance and Systolic Function From the SEAS Substudy

This study sought to assess the impact of valvuloarterial impedance on left ventricular (LV) myocardial systolic function in asymptomatic aortic valve stenosis (AS). In atherosclerotic AS, LV global load consists of combined valvular and arterial resistance to LV ejection. Global load significantly impacts LV ejection fraction (EF) in symptomatic AS, but less is known about its effect on LV myocardial function in asymptomatic AS. Echocardiograms in 1,591 patients with asymptomatic AS (67 +/- 10 years, 51% hypertensive) at baseline in the SEAS (Simvastatin Ezetimibe in Aortic Stenosis) study evaluating placebo-controlled combined simvastatin and ezetimibe treatment in AS were used to assess LV global load as valvuloarterial impedance and LV myocardial function as stress-corrected midwall shortening. The study population was divided into tertiles of global load. Stress-corrected midwall shortening was considered low if <87% in men and <90% in women. Low-flow AS was defined as stroke volume index <22 ml/m(2.04). Energy loss index decreased (0.85 cm(2)/m(2) vs. 0.77 and 0.75 cm(2)/m(2)) and the prevalence of low stress-corrected midwall shortening increased (10% vs. 26% and 63%) with increasing LV global load (all p < 0.001). The EF was low in only 2% of patients. Patients with low-flow AS had higher LV global load and more often low midwall shortening than those with normal-flow AS (9.66 +/- 2.23 mm Hg/ml.m(2.04) and 77%, vs. 6.38 +/- 2.04 mm Hg/ml.m(2.04) and 30%, respectively, p < 0.001). In logistic regression analysis, LV global load was a main predictor of low stress-corrected midwall shortening independent of male sex, concentric LV geometry, LV hypertrophy (all p < 0.001), concomitant hypertension, and aortic regurgitation. LV global load impacts LV myocardial function in asymptomatic AS independent of other main covariates of LV systolic function. LV myocardial systolic dysfunction is common in asymptomatic AS in particular in patients with low-flow AS and increased valvuloarterial afterload, whereas EF is generally preserved. (An Investigational Drug on Clinical Outcomes in Patients With Aortic Stenosis [Narrowing of the Major Blood Vessel of the Heart]; NCT00092677).

Compensatory or inappropriate left ventricular mass in different models of left ventricular pressure overload: comparison between patients with aortic stenosis and arterial hypertension

Aortic valve stenosis and arterial hypertension (AH) are two models of left ventricular (LV) pressure overload, which commonly induce increase in LV mass. Prevalence and predictors of excess of LV mass (inappropriate LVM) has been recently investigated in AH patients. Whether or not this phenomenon also exists in patients with aortic valve stenosis has to be defined. To evaluate prevalence of and factors associated with inappropriate LVM as a response to overload in aortic valve stenosis compared to AH patients. One hundred patients with aortic valve stenosis (mean valve area 0.67 +/- 0.18 cm/m) were studied by Doppler echocardiography and compared to 200 patients with AH. Inappropriate LVM was diagnosed when the measured LV mass exceeded by 28% the expected value predicted from height, sex and stroke work. Prevalence of inappropriate LVM was similar in aortic valve stenosis (n: 24 = 24%) and AH patients (n: 55 = 27.5%). Aortic valve stenosis had greater LVM (203 +/- 57 vs. 182 +/- 53 g, P = 0.001), more concentric LV geometry, lower midwall shortening and higher left atrial systolic force than AH. In both study groups, high LV mass, concentric LV geometry and reduced systolic function emerged as independent correlates of inappropriate LV mass. Although LV and left atrial geometric adaptation in aortic valve stenosis is different from AH, reflecting a near-pure pressure overload, aortic valve stenosis patients have a prevalence of inappropriately high LVM which is similar to those with AH. Geometric and functional characteristics of inappropriate LVM do not differ in aortic valve stenosis and AH, despite the different loading conditions.

Impaired Inotropic Response in Type 2 Diabetes Mellitus: A Strain Rate Imaging Study

Left ventricular (LV) concentric geometry and hypertrophy, depressed wall mechanics, and abnormal diastolic properties have been described in the diabetic heart. However, the cardiac response to dynamic exercise in diabetic patients remains controversial. The present study assessed strain rate (SR) imaging during dobutamine stress, to investigate inotropic response in patients with type 2 diabetes mellitus and without coronary artery disease. Twenty-four diabetics and 16 controls, both free of coronary artery disease, underwent Doppler echocardiography at rest and during dobutamine stress. Tissue Doppler systolic (S(m)) and early diastolic (E(m)) velocities, SR, and strain of middle posterior septum were measured at rest, low-dose, and high-dose dobutamine. Diabetics had higher LV mass and relative wall thickness, lower midwall shortening, and transmitral pattern of abnormal LV relaxation. At rest, E(m) was significantly lower but S(m), SR, and strain were similar between the two groups. At low-dose and high-dose dobutamine, without difference of S(m), SR and strain were significantly lower in diabetics. At every level of dobutamine, strain increased with increasing heart rate (HR) in either group (both P < .0001), but the slope of the overall relation between HR and strain was lower in diabetics (b = -0.08) than in controls (b = -0.14) (P < .01). In type 2 diabetes SR imaging allows detection of reduced longitudinal mechanics during dobutamine stress. The blunted slope of the relation between HR and regional strain suggests the impairment of the myocardial force-frequency relation, indicating altered contractile reserve in uncomplicated diabetes.

1039 The impact of using different measures of relative wall thickness on assessment of left ventricular geometry in asymptomatic aortic stenosis. A SEAS substudy

in men/women), RWT and midwall shortening were evaluated in 1728 patients (39% women, aged 67±10 years) with asymptomatic AS, re- cruited in the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) study. RWT was defined as the ratio of either posterior wall thickness (RWTp, concentric geometry if ≥0.43), or the average of posterior and septal wall thickness (RWTm, concentric geometry if ≥0.45) to LV radius. Both variables were also normalized for age using previously published regression coefficients (RWTpa and RWTma, concentric geometry if ≥0.40 and 0.41, respectively). Results: Average peak transaortic velocity was 3.09±0.54 m/sec. Compared to RWTp and RWTm, use of RWTpa and RWTma reclassified LV geometry in 2.8% and 3.5% of patients (Table 1). Compared to RWTp, use of RWTm reclassified LV geometry in 11.2% of patients (183 from eccentric to concen- tric and 11 from concentric to eccentric geometry) (p<0.01). Compared to those who maintained eccentric or concentric geometry, respectively, pa- tients reclassified to concentric geometry by RWTm included more hyper- tensive patients, had larger LV mass and wall thicknesses and lower midwall shortening (all p<0.05), while patients reclassified to eccentric geometry did not differ in clinical characteristics, but had lower LV septal thickness and higher midwall shortening (both p<0.01). Conclusions: Use of age-normalized RWT modestly reclassified LV geom- etry in this elderly population. However, in patients with asymptomatic AS, defining RWT from average septal and posterior wall thickness compared to posterior wall thickness alone, considerably increased both prevalence of concentric geometry and associated midwall dysfunction. ), with low gradient-low EF (LVEF £35%, GDT £30 mm Hg) and who had aortic valvular replacement (AVR) were prospectively enrolled. Preoperative contractile reserve (CR) during dobutamine infusion was defined by an increase in stroke volume of ≥20% compared with baseline values. CR was present in 35 patients (Group I, 76%) and absent in 11 patients (Group II, 24%). In the overall sample, operative mortality was 17%. Operative mortality was 8.5% in group I compared with 45% in group II (p=0.013). In univariate analysis, lack of CR (p=0.013), three-vessel coronary artery disease (p=0.02) and GDT £20 mm Hg (p=0.02) were associated with operative mortality. In- dependent predictors of operative mortality were GDT £20 mmHg (odds ra- tio=11; 95% CI, 1.2 to 107.6; p=0.03), lack of contractile reserve (odds ratio =10; 95% CI, 1.2 to 81.6; p=0.034) and three vessels coronary artery disease (odds ratio =11; 95% CI, 1.2 to 107.6; p=0.034). All patients without CR and with GDT £20 mmHg (n=3) died in the perioperative period. Conclusions: These data further support in patients with low GDT-low EF AS the value of very low gradient (±20 mm Hg) at rest and of CR on DSH for preoperative risk stratification. Patients with GDT £20 mm Hg and lack of CR have an extremely high operative mortality.

Relation between left ventricular midwall function and coronary vasodilator capacity in arterial hypertension.

In systemic hypertension, depressed left ventricular midwall shortening predicts an adverse outcome and is associated with increased left ventricular relative wall thickness, which has been proposed as an independent predictor of cardiovascular risk and reduced coronary reserve. This study was designed to investigate whether depressed midwall shortening is associated with more critical impairment of coronary function and with exercise-induced myocardial ischemia. Sixty untreated hypertensive patients without coronary artery stenosis and 20 normotensive volunteers underwent exercise ECG testing, standard and transesophageal echocardiography to assess the occurrence of exercise-induced myocardial ischemia, left ventricular mass, geometry, and midwall shortening, and coronary vasodilator capacity. Compared with hypertensive patients with normal midwall shortening, those with depressed function (n=15) had higher minimum coronary resistance (1.19+/-0.27 versus 1.39+/-0.20 mm Hg/cm per second, P<0.01) and prevalence of exercise-induced myocardial ischemia (36 versus 67%, P<0.05). Within the hypertensive group, midwall shortening was inversely related to minimum coronary resistance (r=-0.42, P<0.01). Compared with patients with an exercise ECG test negative for myocardial ischemia, those with a positive test result (n=26) had higher minimum coronary resistance (1.13+/-0.21 versus 1.38+/-0.27 mm Hg/cm per second, P<0.01) and lower midwall shortening (104+/-16 versus 93+/-14%, P<0.01). We conclude that hypertensive patients with depressed midwall shortening have more severe impairment of coronary function and a higher prevalence of exercise-induced myocardial ischemia as compared with hypertensive patients with normal midwall shortening. These findings suggest that a decrease in myocardial performance may be related, at least in part, to chronic intermittent myocardial ischemia caused by a critical impairment of coronary vasodilator capacity.

Midwall Left Ventricular Mechanics

An appreciable proportion of asymptomatic hypertensive patients have depressed left ventricular (LV) performance that is identified by midwall shortening/endsystolic stress relations but not by indexes that use endocardial shortening. It has not been established, however, whether depressed midwall ventricular performance has prognostic implications. Echocardiographic endocardial and midwall LV fractional shortening/circumferential end-systolic stress relations in 294 hypertensive patients were analyzed as predictors of the occurrence of cardiovascular morbid events that occurred in 50 patients (including 14 deaths) during a 10-year mean follow-up. Patients with initially lower midwall but not endocardial shortening, either in absolute terms or as a percentage of predicted from observed end-systolic stress, were more likely to suffer morbid events than those with initially normal values (P < .004). Cardiovascular events occurred in 29 of 100 patients (29%) and death in 10 of 100 patients (10%) among those who were in both the two highest quartiles of LV mass index and the two lowest quartiles of midwall shortening, as opposed to 21 of 194 (11%) and 4 of 194 (2.1%) of the remaining patients (odds ratio, 3.4; 95% CI, 1.8 to 6.3; P < .0001; and odds ratio, 5.3; 95% CI, 1.6 to 17.3; P < .006, respectively). In logistic analysis, increasing age, high LV mass, high systolic blood pressure, and low values for an interaction term between LV mass index and midwall shortening independently predicted cardiovascular events (.04 < P < .001); increasing age, low midwall LV shortening as a percentage of predicted, and high value of the interaction term predicted the occurrence of cardiac death (.004 < P < .0002). Survival analysis controlling for age confirmed that low midwall shortening independently predicted cardiac morbidity or death, especially in the subgroup of patients with LV hypertrophy. Depressed midwall shortening is a predictor of adverse outcome in arterial hypertension; the combination of higher LV mass and lower midwall shortening identifies individuals at markedly increased risk.