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Background: B-lines detected by lung ultrasound (LUS) during exercise stress echocardiography (ESE), indicating pulmonary congestion, have not been systematically evaluated in patients with hypertrophic cardiomyopathy (HCM)., Aim: To assess the clinical, anatomical and functional correlates of pulmonary congestion elicited by exercise in HCM., Methods: We enrolled 128 HCM patients (age 52 ± 15 years, 72 males) consecutively referred for ESE (treadmill in 46, bicycle in 82 patients) in 10 quality-controlled centers from 7 countries (Belgium, Brazil, Bulgaria, Hungary, Italy, Serbia, Spain). ESE assessment at rest and peak stress included: mitral regurgitation (MR, score from 0 to 3); E/e'; systolic pulmonary arterial pressure (SPAP) and end-diastolic volume (EDV). Change from rest to stress was calculated for each variable. Reduced preload reserve was defined by a decrease in EDV during exercise. B-lines at rest and at peak exercise were assessed by lung ultrasound with the 4-site simplified scan. B-lines positivity was considered if the sum of detected B-lines was ≥ 2., Results: LUS was feasible in all subjects. B-lines were present in 13 patients at rest and in 38 during stress (10 vs 30%, p < 0.0001). When compared to patients without stress B-lines (n = 90), patients with B-lines (n = 38) had higher resting E/e' (14 ± 6 vs. 11 ± 4, p = 0.016) and SPAP (33 ± 10 vs. 27 ± 7 mm Hg p = 0.002). At peak exercise, patients with B-lines had higher peak E/e' (17 ± 6 vs. 13 ± 5 p = 0.003) and stress SPAP (55 ± 18 vs. 40 ± 12 mm Hg p < 0.0001), reduced preload reserve (68 vs. 30%, p = 0.001) and an increase in MR (42 vs. 17%, p = 0.013) compared to patients without congestion. Among baseline parameters, the number of B-lines and SPAP were the only independent predictors of exercise pulmonary congestion., Conclusions: Two-thirds of HCM patients who develop pulmonary congestion on exercise had no evidence of B-lines at rest. Diastolic impairment and mitral regurgitation were key determinants of pulmonary congestion during ESE. These findings underscore the importance of evaluating hemodynamic stability by physiological stress in HCM, particularly in the presence of unexplained symptoms and functional limitation., (© 2022. The Author(s).)

Objective: We aimed to assess feasibility and functional correlates of left atrial volume index (LAVI) changes during exercise stress echocardiography (ESE)., Methods: ESE on a bike or treadmill was performed in 363 patients with heart failure with preserved ejection fraction (HFpEF, n = 173), reduced ejection fraction (HFrEF, n = 59), or hypertrophic cardiomyopathy (HCM, n = 131). The LAVI stress-rest increase ≥6.8 ml/m 2 was defined as dilation., Results: LAVI measurements were feasible in 100%. LAVI did not change in HFrEF being at rest 32 (25-45) vs at stress 36 (24-54) ml/m 2 , P = NS and in HCM at rest 35 (26-48) vs at stress 38 (28-48) ml/m 2 , P = NS, whereas it decreased in HFpEF from 30 (24-40) to 29 (21-37) ml/m 2 at stress, P = 0.007. LA dilation occurred in 107 (30%) patients (27% with treadmill vs 33% with bike ESE, P = NS): 26 with HFpEF (15%), 26 with HFrEF (44%), and 55 with HCM (42%) with P < 0.001 for HFrEF and HCM vs HFpEF. A multivariate analysis revealed as the predictors for LAVI dilation E/e' > 14 at rest with odds ratio (OR) 4.4, LVEF <50% with OR 2.9, and LAVI at rest <35 ml/m 2 with OR 2.7., Conclusion: The LAVI assessment during ESE was highly feasible and dilation equally frequent with a treadmill or bike. LA dilation was three-fold more frequent in HCM and HFrEF and could be predicted by increased resting E/e' and impaired EF as well as smaller baseline LAVI., Competing Interests: Conflict of interest There is no conflict of interest., (Copyright © 2022 Hellenic Society of Cardiology. Published by Elsevier B.V. All rights reserved.)

Background: Stress echo (SE) may have a role in the outcome in patients with hypertrophic cardiomyopathy (HCM)., Objectives: The aim was to assess the prognostic value of SE in a retrospective multicenter study in HCM., Methods: We enrolled 706 HCM patients. The employed stress was exercise (n=608) and/or vasodilator (n=146, dipyridamole in 98 and adenosine in 48). We defined SE positivity according to clinical/hemodynamic criteria including: symptoms (all stress modalities), exercise-induced hypotension (failure to increase or fall >20mmHg, exercise) and exercise-induced left ventricular outflow tract obstruction (left ventricular outflow tract obstruction >50mmHg); and ischemic criteria, such as new wall motion abnormalities (new wall motion abnormality) and/or reduction of coronary flow reserve velocity (CFVR≤2.0) on left anterior descending coronary artery with vasodilator stress assessed in 116 patients. All patients completed the clinical follow-up., Results: Positive SE showed more frequently CFVR reduction, exercise-induced hypotension, left ventricular outflow tract obstruction, and symptoms (38, 23, 20 and 15% respectively), but new wall motion abnormality only in 6%. During a median follow-up of 49months 180 events were observed, including 40 deaths. Clinical/hemodynamic criteria did not predict outcome (X2 0.599, p=0.598), whereas ischemia-related SE criteria (X2: 111.120, p<0.0001) was significantly related to outcome. Similarly, mortality was predicted with SE ischemic-criteria (X2 16.645, p<0.0001)., Conclusions: SE has an important prognostic significance in HCM patients, with ischemia-related end-points showing greater predictive accuracy than hemodynamic endpoints. New wall motion abnormalities and impairment of CFVR should be specifically included in SE protocols for HCM., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Background: Abnormal blood-pressure response during exercise occurs in about one third of patients with hypertrophic cardiomyopathy (HCM), and it has been associated with a high risk of sudden cardiac death. We assessed the hemodynamics of exercise in HCM patients with abnormal blood-pressure response by using ambulatory radionuclide monitoring (VEST) of left-ventricular (LV) function, and exercise tolerance by oxygen consumption., Methods: Twenty-two HCM patients underwent treadmill exercise during VEST monitoring. A cardiopulmonary exercise test was performed a few days after. The VEST data were averaged for 1 minute. Stroke volume, cardiac output, and systemic vascular resistance were expressed as percent of baseline. Exercise tolerance was assessed as maximal oxygen consumption., Results: In eight HCM patients (36%) with an abnormal blood-pressure response, end-systolic volume increased more (52% +/- 21% vs 31% +/- 28%, P = .012), and the ejection fraction (-31% +/- 17% vs -14% +/- 22%, P = .029) and stroke volume (-21% +/- 21% vs 3% +/- 28%, P = .026) fell more, than in patients with normal response. Cardiac output increased less in the former patients (49% +/- 44% vs 94% +/- 44%, P = .012). Systemic vascular resistance decreased similarly, irrespective of blood-pressure response (-28% +/- 26% vs -34% +/- 26%, P = N.S.). Percent of maximal predicted oxygen consumption was lower in HCM patients with an abnormal blood-pressure response (63% +/- 11% vs 78% +/- 15%, P = .025)., Conclusions: In HCM patients, abnormal blood-pressure response was associated with exercise-induced LV systolic dysfunction and impairment in oxygen consumption. This may cause hemodynamic instability, associated with a high risk of sudden cardiac death.

Aim: The aim of the present study was to evaluate [123I] MIBG uptake and clearance in patients with hypertrophic cardiomyopathy (HCM) and to assess their relationships with left ventricular function (systolic and diastolic) and perfusion., Methods: Eleven consecutive patients with HCM (8 men and 3 women; mean age 38+/-12 years, none in the dilated phase) underwent (in separate days, in random order) [123I]-MIBG scintigraphy, [(99m)Tc]-MIBI SPET at rest, and echocardiography. All patients were studied in fasting condition, and all medications were discontinued. [(99m)Tc]-MIBI SPET study was performed 1 hour after tracer injection. [123I]-MIBG study was acquired 5 minutes (planar) and 4 hours (planar and SPET) after the i.v. injection of [123I]-MIBG. Heart to mediastinum ratio (H/M) was computed at 4 hours. Wash out rate (WOR) was computed as: (H early - H delayed)/(H early), after decay correction. Both [123I]-MIBG and [(99m)Tc]-MIBI SPET were analyzed on 3 short axis views (apical, middle, and basal). Left ventricular outflow tract gradient (LVOTG), ejection fraction, volumes, septum thickness, and left atrial fractional shortening (LAFS) were evaluated on echocardiography., Results: [123I]-MIBG WOR showed a positive relationship with LVOTG (r=0.84, p<0.001) and septum thickness (r=0.76, p<0.01), while a negative one was found with LAFS (r= -0.66, p<0.05). The study group was divided into: Group A (n=5) with higher, and Group B (n=6) with lower WOR than the median value (i.e. 11%). Group A patients had significantly lower LAFS (17.6+/-4.8 vs 26.8+/-7.2%, p<0.05), higher LVOTG (49+/-35 vs 3+/-3 mmHg), and thicker septum (21+/-2 vs 17+/-2 mm) than Group B patients. Inferior and septal wall [123I]-MIBG uptake on 4 hour SPET was significantly lower in Group A than in Group B. On the other hand, no differences were found in (99m)T-MIBI SPET rest regional uptake between the 2 subgroups of patients., Conclusion: These results suggest that cardiac sympathetic activity correlates to cardiac anatomy (i.e. degree of hypertrophy) and diastolic function in patients with HCM.

Background: Myocardial interstitial fibrosis is a characteristic of hypertrophic cardiomyopathy (HCM). This study evaluates the collagen turnover in HCM and its impact on left ventricular (LV) diastolic function., Methods and Results: Thirty-six HCM patients and 14 sex- and age-matched controls were studied. Collagen turnover was assessed as follows. By radioimmunoassay, a byproduct of collagen III synthesis (PIIINP) and 3 peptides resulting from collagen I synthesis (PICP and PINP) and degradation (ICTP) were measured. By ELISA, matrix metalloproteinases (MMPs) were determined, as follows: active MMP-2; active MMP-9; and MMP-1 as active, free (as active MMP-1 plus its precursor), and total (as free MMP-1 plus MMP-1/tissue inhibitor complexes). Tissue inhibitor of metalloproteinases-1 (TIMP-1) was also assayed. All patients underwent echocardiography. The difference in duration between transmitral forward (A) and pulmonary venous retrograde (AR) waves (A-Ar) was considered an estimate of passive diastolic function. Furthermore, restrictive or pseudonormal LV filling patterns were considered to identify patients with passive diastolic dysfunction. Patients had higher levels of PIIINP, ICTP, MMP-2, MMP-9, and total TIMP-1 than did controls. PIIINP was inversely related to LV end-diastolic diameter. A-Ar was inversely related to PICP, PINP, and their differences with ICTP (estimates of collagen I buildup). Furthermore, A-Ar was directly related to MMP-1 and MMP-2., Conclusions: As compared with controls, collagen turnover is enhanced in HCM patients. As collagen I synthesis prevails over degradation and MMP-1 and MMP-2 are inhibited, passive diastolic dysfunction occurs in patients with HCM.

Background: We assessed the hemodynamic effects of isometric exercise by an ambulatory radionuclide monitoring device (VEST) that measured left ventricular function in patients who had hypertrophic cardiomyopathy (HCM), with and without significant left ventricular outflow-tract obstruction at rest, compared with control subjects., Methods and Results: We studied 10 patients with obstructive HCM, 25 patients with nonobstructive HCM, and 11 control subjects. During VEST monitoring, all patients gripped a dynamometer at 75% of maximal strength for up to 5 minutes. End-diastolic, end-systolic, and stroke volumes; cardiac output; and systemic vascular resistance were expressed as a percentage of baseline. The mean exercise duration was similar among the 3 groups. During handgrip, heart rate, systolic blood pressure, and cardiac output increased significantly and similarly in the 3 groups. There was a significant difference in the lung activity between obstructive and nonobstructive HCM patients and control subjects (P <.001), with a fall in control subjects and no change in HCM patients, irrespective of obstruction. Control subjects showed a decrease in end-systolic volume (P =.02) and an increase in ejection fraction (P =.003) and stroke volume (P =.009), whereas these parameters did not change in HCM patients, irrespective of obstruction. Systemic vascular resistance increased in obstructive (P =.02) and nonobstructive (P <.01) HCM patients but did not change in control subjects., Conclusions: Isometric exercise causes an abnormal and similar adaptation to load changes in obstructive and nonobstructive HCM patients, as compared with control subjects.

Aims: Myocardial ischemia in the absence of coronary artery disease is common in patients with hypertrophic cardiomyopathy (HCM). Dobutamine stress echocardiography (DSE) induces left ventricular (LV) new wall motion abnormalities (NWMA) in some patients with HCM. We evaluated the effects of dobutamine on LV performance and hemodynamics in HCM., Methods and Results: Eighteen patients with non-obstructive HCM underwent DSE. Dobutamine was administered at dosages of 5, 10, 20, 30 and 40 microg/kg/min with increments at intervals of 3 min. Seven patients developed NWMA, whereas the other 11 did not. During DSE, heart rate increased significantly more in NWMA patients,whereas LV outflow tract gradient (OTG) increased significantly and similarly in both groups. At peak dobutamine dose, NWMA patients had a significant increase in LV end-systolic diameter and volume and a significant decrease in LV fractional shortening and ejection fraction. Posterior wall thickening increased significantly, whereas septal thickening did not increase throughout DSE in both groups., Conclusions: In a subgroup of patients with HCM, DSE induces NWMA, associated with a greater increase in heart rate, irrespective of LVOTG. NWMA induce a depression of global LV systolic performance. The septum shows no contractile reserve, regardless of NWMA. These phenomena may be the result of induction of ischemia and/or impaired LV systolic function due to fast heart rate., (Copyright 2003 S. Karger AG, Basel)

Objectives: We sought to assess the hemodynamics of exercise in patients with hypertrophic cardiomyopathy (HCM), with and without an exercise-induced abnormal blood pressure (BP) response, by ambulatory radionuclide monitoring of left ventricular (LV) function with the VEST device (Capintec Inc., Ramsey, New Jersey)., Background: Blood pressure fails to increase >20 mm Hg during exercise in about one-third of patients with HCM. This carries a high risk of sudden death., Methods: Forty-three patients with HCM and 14 control subjects underwent maximal symptom-limited exercise on a treadmill during VEST. The VEST data were averaged for 1 min and analyzed at baseline, 3 min and peak exercise. The LV end-diastolic, end-systolic and stroke volumes, cardiac output and systemic vascular resistance were expressed as the percentage of baseline., Results: Ejection fraction and stroke volume fell in patients with HCM, although they increased in control subjects (p < 0.001 and p = 0.002, respectively). Cardiac output increased significantly more in control subjects than in patients with HCM (p = 0.001). In 17 patients with HCM (39%) with an abnormal BP response, ejection fraction and stroke volume fell more (p = 0.032 and p = 0.009, respectively) and cardiac output increased less (p = 0.001) than they did in patients with HCM with a normal BP response. Systemic vascular resistance decreased similarly in patients with HCM, irrespective of the BP response., Conclusions: In patients with HCM with and without an abnormal BP response, abnormal hemodynamic adaptation to exercise was qualitatively similar but quantitatively different. An abnormal BP response was associated with exercise-induced LV systolic dysfunction. This causes hemodynamic instability, associated with a high risk of sudden cardiac death.

This study was designed to investigate whether, in patients with hypertrophic cardiomyopathy (HC), tilt-induced volume unloading triggers a peripheral reflex similar to that seen in patients with a history of vasovagal syncope or rather acts through an intrinsic cardiac mechanism secondary to diastolic dysfunction. Thirty-seven patients with HC (10 with and 27 without a history of syncope), 10 patients with vasovagal syncope, and 9 controls underwent 70 degrees head-up tilt for 45 minutes during continuous radionuclide monitoring of left ventricular function. We focused on the initial 5 minutes into the tilt test, well before symptoms occurred, to exclude that the observed hemodynamic changes were the consequence rather than the cause of syncope. HC patients with previous syncope and vasovagal patients experienced significant hypotension after the initial 5 minutes of tilt. Only HC patients with a history of syncope had a significant decrease in cardiac output, which began at the initial stage of the test. Systemic vascular resistance decreased in vasovagal patients, but increased in the HC syncopal group. Baseline peak filling rate was lower (2.4 +/- 0.5 vs 3.3 +/- 1.1 stroke counts/s, p = 0.03) and a "pseudonormal" or a restrictive pattern of left ventricular filling was more frequent (70% vs 26%, p = 0.02) in HC patients with than without a history of syncope. Thus, significant hypotension or frank syncope during orthostatic stress in HC patients with a history of syncope is due to an early decrease in cardiac output, which occurs well before the onset of symptoms; such impaired hemodynamic adaptation seems to be related to diastolic dysfunction.

Aims: Atrial and brain natriuretic peptide levels closely reflect impaired left ventricular function in patients with heart failure. In the present study we assessed the determinants and the clinical significance of atrial and brain natriuretic peptide plasma levels in hypertrophic cardiomyopathy., Methods and Results: In 44 patients with hypertrophic cardiomyopathy (40+/-15 years) we evaluated: (a) atrial and brain natriuretic peptide plasma levels; (b) left ventricular hypertrophy; (c) left ventricular ejection fraction; (d) transmitral and pulmonary venous flow velocity patterns, and left atrial fractional shortening; (e) left ventricular outflow tract gradient; (f) maximal oxygen consumption. Left ventricular hypertrophy influenced only brain natriuretic peptide levels (r=0.32;P<0.05). Atrial and brain natriuretic peptide plasma levels did not correlate with left ventricular ejection fraction, but correlated with left ventricular outflow tract gradient (r=0.35;P<0.05; and r=0.40, P=0.022, respectively) and left atrial fractional shortening (r=-0.57;P<0.001, and r=-0.35;P<0.05, respectively). Atrial but not brain natriuretic peptide plasma levels were inversely related to maximal oxygen consumption (r=-0.35;P<0.05). By stepwise multiple regression analysis, left atrial fractional shortening and left ventricular outflow tract gradient were the only predictors of atrial and brain natriuretic peptide plasma levels, respectively., Conclusions: In hypertrophic cardiomyopathy, atrial natriuretic peptide plasma levels are mainly determined by diastolic function: this explains the relationship with exercise tolerance. In contrast, brain natriuretic peptide plasma levels are mainly determined by left ventricular outflow tract gradient., (Copyright 2001 The European Society of Cardiology.)

Some studies have demonstrated that left ventricular (LV) diastolic function is the principal determinant of impaired exercise capacity in hypertrophic cardiomyopathy (HC). In this study we sought the capability of echocardiographic indexes of diastolic function in predicting exercise capacity in patients with HC. We studied 52 patients with HC while they were not on drugs;12 of them had LV tract obstruction at rest. Diastolic function was assessed by M-mode and Doppler echocardiography by measuring: (1) left atrial fractional shortening, and the slope of posterior aortic wall displacement during early atrial emptying on M-mode left atrial tracing; and (2) Doppler-derived transmitral and pulmonary venous flow velocity indexes. Exercise capacity was assessed by maximum oxygen consumption by cardiopulmonary test during cycloergometer upright exercise. Maximum oxygen consumption correlated with the left atrial fractional shortening (r = 0.63, p <0.001), the slope of posterior aortic wall displacement during early atrial emptying (r = 0.55, p <0.001), age (r = -0.50; p <0.001), pulmonary venous diastolic anterograde velocity (r = 0.41, p <0.01), and the systolic filling fraction (r = -0.43; p <0.01). By stepwise multiple linear regression analysis, left atrial fractional shortening and the pulmonary venous systolic filling fraction were the only determinants of the maximum oxygen consumption (multiple r = 0.70; p <0.001). Exercise capacity did not correlate with Doppler-derived transmitral indexes. Thus, in patients with HC, exercise capacity was determined by passive LV diastolic function, as assessed by the left atrial M-mode and Doppler-derived pulmonary venous flow velocities.

The aim of this study was to assess whether left ventricular (LV) cavity size relates to functional impairment and syncope in patients with hypertrophic cardiomyopathy (HC). LV diastolic dysfunction influences functional limitation in HC. A reduced LV end-diastolic dimension may underlie impaired diastolic properties and be implicated in hemodynamic syncope. Eighty-two consecutive patients with HC (off drugs, in sinus rhythm) underwent echocardiography to measure LV end-diastolic dimension in the short-axis view (indexed to the body surface area) and radionuclide angiography (n = 50) to calculate peak filling rate (normalized to stroke counts/s). Patients in New York Heart Association functional classes II to IV had smaller LV end-diastolic dimension (23.2 +/- 2.6 vs 25.5 +/- 2.5 mm/M2, p = 0.0001) and lower peak filling rate (4.3 +/- 1.4 vs 5.1 +/- 1.3 stroke counts/s, p = 0.036) than those in New York Heart Association class I. LV end-diastolic diameter was correlated to peak filling rate (r = 0.37; p = 0.008). The most potent predictors of functional limitation were LV end-diastolic dimension (relative risk [RR] 0.63, confidence interval [CI] 0.45 to 0.88; p = 0.008), age (RR 1.09, CI 1.03 to 1.17; p = 0.003), and LV thickness score (RR 1.08, CI 1.02 to 1.13; p = 0.003). LV cavity size was smaller in patients with functional limitation irrespective of obstruction and hypertrophy. Patients with differed from those without a history of syncope for a smaller LV end-diastolic dimension (23.2 +/- 2.5 vs 25.0 +/- 2.7 mm/M2, p = 0.008), which was the only independent predictor of syncope (RR 0.77, CI 0.63 to 0.95; p = 0.013). Thus, a small LV cavity size is associated with functional limitation and history of syncope in HC.

Aims: The left ventricle in hypertrophic cardiomyopathy is anatomically and functionally non-uniform. This study was undertaken to verify whether a heterogeneity in the pattern of diastolic filling can be detected along the left ventricular inflow tract in hypertrophic cardiomyopathy., Methods and Results: Early (E) and late (A) diastolic velocities were recorded by Doppler echocardiography at mitral and at mid-ventricular level in 16 normal volunteers and 30 patients with hypertrophic cardiomyopathy. Patients with hypertrophic cardiomyopathy also underwent radionuclide angiography to assess left ventricular function. E wave decreased significantly in normal volunteers (80 +/- 15 to 60 +/- 14 cm x s(-1); P<0.001), but it increased in hypertrophic cardiomyopathy (76 +/- 22 to 87 +/- 28 cm x s(-1) P=0.04), whereas the A wave decreased similarly in both. By multivariate analysis, systolic asynchrony and the ejection fraction of left ventricular lateral wall were directly related to the pattern of early filling progression (r=0.656, F=9.467; P<0.002). Moreover, systolic asynchrony showed a univariate direct correlation with changes in E velocity (r=0.42; P=0.02)., Conclusion: Many patients with hypertrophic cardiomyopathy have an acceleration of filling within the left ventricular inflow tract; this phenomenon is directly related to systolic asynchrony and ejection fraction of the left ventricular lateral wall, suggesting increased suction.

The impact of the duration of atrioventricular (AV) delay on obstruction in hypertrophic cardiomyopathy was evaluated in 12 patients by cardiac catheterization, and in 8 of them also by Doppler echocardiography. The AV delay was programmed in random order at 125, 100 and 75 ms in the invasive study and at 120, 100 and 80 ms after pacemaker implantation. The arterial pressure did not changed throughout the studies, whereas the gradient decreased significantly by reducing the AV delay value; the greater gradient reduction was obtained, in both studies, with the AV delay set between 75 or 80 and 100 ms. QRS duration increased significantly by reducing the AV delay during both studies. The widest QRS was not associated with the smallest gradient in all patients. Changes in gradients were similar during the invasive and noninvasive protocols.

Hypertrophic cardiomyopathy (HC) is characterized by impaired diastolic function, and left ventricular (LV) outflow tract obstruction in about one-fourth of patients. Verapamil improves diastolic properties, but may have dangerous adverse effects. This study investigates the effects of diltiazem on hemodynamics and LV function in 16 patients with HC who were studied with cardiac catheterization and simultaneous radionuclide angiography. Studies were performed during atrial pacing (15 beats above spontaneous rhythm) at baseline and during intravenous diltiazem administration (0.25 mg x kg(-1) over 2 minutes, and 0.014 mg x kg(-1) x min(-1). Diltiazem induced a systemic vasodilation (cardiac index: 3.4 +/- 1.0 to 4.0 +/- 1.0 L x min(-1) x m(-2), p = 0.003; aortic systolic pressure: 116 +/- 16 to 107 +/- 19 mm Hg, p = 0.007; systemic resistance index: 676 +/- 235 to 532 +/- 193 dynes x s x cm(-5) x m(-2), p = 0.006), not associated with changes in the LV outflow tract gradient. The end-systolic pressure/volume ratio decreased (30 +/- 42 to 21 +/- 29 mm Hg x ml(-1) x m(-2); p = 0.044). Pulmonary artery wedge pressure (11 +/- 5 to 15 +/- 6 mm Hg, p = 0.006), and peak filling rate increased (4.1 +/- 1.3 to 6.0 +/- 2.4 stroke counts x s(-1), p = 0.004). The time constant of isovolumetric relaxation tau decreased (74 +/- 40 to 59 +/- 38 ms, p = 0.045). The constant of LV chamber stiffness did not change. Thus, active diastolic function is improved by the acute administration of diltiazem by both direct action and changes in hemodynamics and loading conditions. LV outflow tract gradient does not increase despite systemic vasodilation. In some patients, however, a marked increase in obstruction and a potentially harmful elevation in pulmonary artery wedge pressure do occur. Passive diastolic function is not affected.