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Left ventricular (LV) circumferential strain and rotation have been introduced as clinical markers of myocardial function. This study investigates how regional LV apical rotation and strain can be used in combination to assess function in the infarcted ventricle. In healthy subjects (n = 15) and patients with myocardial infarction (n = 23), LV apical segmental rotation and strain were measured from apical short-axis recordings by speckle tracking echocardiography (STE) and MRI tagging. Infarct extent was determined by late gadolinium enhancement MRI. To investigate mechanisms of changes in strain and rotation, we used a mathematical finite element simulation model of the LV. Mean apical rotation and strain by STE were lower in patients than in healthy subjects (9.0 [+ or -] 4.9 vs. 12.9 [+ or -] 3.5[degrees] and -13.9 [+ or -]10.7 vs. -23.8 [+ or -] 2.3%, respectively, P < 0.05). In patients, regional strain was reduced in proportion to segmental infarct extent (r = 0.80, P < 0.0001). Regional rotation, however, was similar in the center of the infarct and in remote viable myocardium. Minimum and maximum rotations were found at the infarct borders: minimum rotation at the border zone opposite to the direction of apical rotation, and maximum rotation at the border zone in the direction of rotation. The simulation model reproduced the clinical findings and indicated that the dissociation between rotation and strain was caused by mechanical interactions between infarcted and viable myocardium. Systolic strain reflects regional myocardial function and infarct extent, whereas systolic rotation defines infarct borders in the LV apical region. Regional rotation, however, has limited ability to quantify regional myocardial dysfunction. myocardial infarction; myocardial strain; left ventricular function; left ventricular torsion

The present study introduces a new clinical method to define left ventricular (LV) end systole (ES) during tissue Doppler imaging (TDI). Preliminary experiments showed a sharp inflection point in strain traces ([S.sub.IP]) from ischemic borderzones, which coincided with onset of a postsystolic shortening wave ([V.sub.PS]) in the velocity trace. In a single-vessel disease model, we investigated whether [S.sub.IP] and [V.sub.PS] may serve as markers of global ES and their mechanism. In six anesthetized dogs we measured LV pressure and myocardial long-axis function by using TDI and sonomicrometry. Ischemia was induced by left anterior descending coronary artery occlusion. ES was defined by the minimum first derivative of LV pressure. TDI and sonomicrometry demonstrated a sharp [S.sub.IP] and [V.sub.PS] at ES in the ischemic borderzone (defined as moderately ischemic myocardium by pressure-dimension loop analysis). Time differences relative to ES ([+ or -] SD) were -0.1 [+ or -] 2.3 (intraclass correlation coefficient [R.sub.IC] = 0.996) and 6.8 [+ or -] 10.7 ms ([R.sub.IC]= 0.89) for [S.sub.IP] as shown by sonomicrometry and TDI, respectively. There was a strong inverse relationship between postsystolic shortening in the borderzone and simultaneous lengthening of nonischemic myocardium. In 30 patients with acute myocardial infarction, [S.sub.IP], and [V.sub.PS] evaluated by TDI were compared with ES defined by aortic valve closure. Time differences were -4 [+ or -] 14 ([R.sub.IC]= 0.94) and -2 [+ or -] 11 ms ([R.sub.IC]= 0.96), respectively. In the ischemic borderzone, [S.sub.IP] and [V.sub.PS] identified global ES with high accuracy. The force balance or 'tug of war' between borderzone and nonischemic myocardium is a likely underlying mechanism for these markers. The method may be used as an 'all in one heart beat' approach for TDI analysis in acute myocardial ischemia. echocardiography; infarction; reperfusion; ventricular function; tissue Doppler imaging

Aims: We aimed to characterize the substrate of T-wave inversion (TWI) using cardiac magnetic resonance (CMR) and the association between diffuse fibrosis and ventricular arrhythmias (VA) in patients with mitral valve prolapse (MVP).Methods and Results: TWI was defined as negative T-wave ≥0.1 mV in ≥2 adjacent ECG leads. Diffuse myocardial fibrosis was assessed by T1 relaxation time and extracellular volume (ECV) fraction by T1-mapping CMR. We included 162 patients with MVP (58% females, age 50 ± 16 years), of which 16 (10%) patients had severe VA (aborted cardiac arrest or sustained ventricular tachycardia). TWI was found in 34 (21%) patients. Risk of severe VA increased with increasing number of ECG leads displaying TWI [OR 1.91, 95% CI (1.04-3.52), P = 0.04]. The number of ECG leads displaying TWI increased with increasing lateral ECV (26 ± 3% for TWI 0-1leads, 28 ± 4% for TWI 2leads, 29 ± 5% for TWI ≥3leads, P = 0.04). Patients with VA (sustained and non-sustained ventricular tachycardia) had increased lateral T1 (P = 0.004), also in the absence of late gadolinium enhancement (LGE) (P = 0.008).Conclusions: Greater number of ECG leads with TWI reflected a higher arrhythmic risk and higher degree of lateral diffuse fibrosis by CMR. Lateral diffuse fibrosis was associated with VA, also in the absence of LGE. These results suggest that TWI may reflect diffuse myocardial fibrosis associated with VA in patients with MVP. T1-mapping CMR may help risk stratification for VA. [ABSTRACT FROM AUTHOR]

There is a need for better methods to quantify regional myocardial function. In the present study, we investigated the feasibility of quantifying regional function in terms of a segmental myocardial work index as derived from strain Doppler echocardiography (SDE) and invasive pressure. In 10 anesthetized dogs, we measured left ventricular (LV) pressure by micromanometer and myocardial longitudinal strains by SDE and sonomicrometry. The regional myocardial work index (RMWI) was calculated as the area of the pressure-strain loop. As a reference method for strain, we used sonomicrometry. By convention, the loop area was assigned a positive sign when the pressure-strain coordinates rotated counterclockwise. Measurements were done at baseline and during volume loading and left anterior descending coronary artery (LAD) occlusion, respectively. There was a good correlation between RMWI calculated from strain by SDE and strain by sonomicrometry (y = 0.73x + 0.21, r = 0.82, P < 0.01). Volume loading caused an increase in RMWI from 1.3 [+ or -] 0.2 to 2.2 [+ or -] 0.1 kJ/[m.sup.3] (P < 0.05) by SDE and from 1.5 [+ or -] 0.3 to 2.7 [+ or -] 0.3 kJ/[m.sup.3] (P = 0.066) by sonomicrometry. Short-term ischemia (1 min) caused a decrease in RMWI from 1.3 [+ or -] 0.2 to 0.3 [+ or -] 0.04 kJ/[m.sup.3] (P < 0.05) and from 1.3 [+ or -] 0.3 to 0.5 [+ or -] 0.2 kJ/[m.sup.3] (P < 0.05) by SDE and sonomicrometry, respectively. In the nonischemic ventricle and during short-term ischemia, the pressure-strain loops rotated counterclockwise, consistent with actively contracting segments. Long-term ischemia (3 h), however, caused the pressure-strain loop to rotate clockwise, consistent with entirely passive segments, and the loop areas became negative, -0.2 [+ or -] 0.1 and -0.1 [+ or -] 0.03 kJ/[m.sup.3] (P < 0.05) by SDE and sonomicrometry, respectively. A RMWI can be estimated by SDE in combination with LV pressure. Furthermore, the orientation of the loop can be used to assess whether the segment is active or passive. sonomicrometry; pressure-strain loop

Acute myocardial ischemia has been associated with abnorreal filling patterns in the left ventricular (LV) apex. We hypothesized that this may in part be due to postsystolic shortening of ischemic apical segments, which leads to reversal of early diastolic apical flow. Fourteen open-chest anesthetized dogs were instrumented with micromanometers in the LV apex and left atrium and myocardial sonomicrometers in the anterior apical LV wall. Intraventricular filling by color Doppler and wall motion by strain Doppler echocardiography (SDE) were assessed from an apical view. Measurements were taken before and after 5 min of left anterior descending coronary artery (LAD) occlusion. In four dogs, we measured the pressure difference between the LV apex and outflow tract. At baseline, peak early diastolic flow velocities in the distal one-third of the LV were directed toward apex (9.2 [+ or -] 1.6 cm/s). After LAD occlusion, the velocities reversed (-2.3 [+ or -] 0.4 cm/s, P < 0.01), indicating that blood was ejected from the apex toward the base during early filling. This interpretation was confirmed by wall motion analysis, which showed postsystolic shortening of apical myocardial segments. The postsystolic shortening represented 9.7 [+ or -] 1.7% (P < 0.01) and 14.2 [+ or -] 2.4% (P < 0.01) of end-diastolic segment length by SDE and sonomicrometry, respectively. Consistent with the velocity changes, we found reversal of the early diastolic pressure gradient from the LV apex to outflow tract. In the present model, acute LAD occlusion resulted in reversal of early diastolic apical flow, and this was attributed to postsystolic shortening of dyskinetic apical segments. The clinical diagnostic importance of this finding remains to be determined. strain-Doppler echocardiography; two-dimensional color Doppler; myocardial ischemia; diastolic filling

Aims: We aimed to assess sex-specific phenotypes and disease progression, and their relation to exercise, in arrhythmogenic cardiomyopathy (AC) patients.Methods and Results: In this longitudinal cohort study, we included consecutive patients with AC from a referral centre. We performed echocardiography at baseline and repeatedly during follow-up. Patients' exercise dose at inclusion was expressed as metabolic equivalents of task (MET)-h/week. Ventricular arrhythmia (VA) was defined as aborted cardiac arrest, sustained ventricular tachycardia, or appropriate therapy by implantable cardioverter-defibrillator. We included 190 AC patients (45% female, 51% probands, age 41 ± 17 years). Ventricular arrhythmia had occurred at inclusion or occurred during follow-up in 85 patients (33% of females vs. 55% of males, P = 0.002). Exercise doses were higher in males compared with females [25 (interquartile range, IQR 14-51) vs. 12 (IQR 7-22) MET-h/week, P < 0.001]. Male sex was a marker of proband status [odds ratio (OR) 2.6, 95% confidence interval (CI) 1.4-5.0, P = 0.003] and a marker of VA (OR 2.6, 95% CI 1.4-5.0, P = 0.003), but not when adjusted for exercise dose and age (adjusted OR 1.8, 95% CI 0.9-3.6, P = 0.12 and 1.5, 95% CI 0.7-3.1, P = 0.30, by 5 MET-h/week increments). In all, 167 (88%) patients had ≥2 echocardiographic examinations during 6.9 (IQR 4.7-9.8) years of follow-up. We observed no sex differences in deterioration of right or left ventricular dimensions and functions.Conclusion: Male AC patients were more often probands and had higher prevalence of VA than female patients, but not when adjusting for exercise dose. Importantly, disease progression was similar between male and female patients. [ABSTRACT FROM AUTHOR]

Background: The response rate to cardiac resynchronization therapy (CRT) may be improved if echocardiographic‐derived parameters are used to guide the left ventricular (LV) lead deployment. Tools to visually integrate deformation imaging and fluoroscopy to take advantage of the combined information are lacking. Methods: An image fusion tool for echo‐guided LV lead placement in CRT was developed. A personalized average 3D cardiac model aided visualization of patient‐specific LV function in fluoroscopy. A set of coronary venography‐derived landmarks facilitated registration of the 3D model with fluoroscopy into a single multimodality image. The fusion was both performed and analyzed retrospectively in 30 cases. Baseline time‐to‐peak values from echocardiography speckle‐tracking radial strain traces were color‐coded onto the fused LV. LV segments with suspected scar tissue were excluded by cardiac magnetic resonance imaging. The postoperative augmented image was used to investigate: (a) registration accuracy and (b) agreement between LV pacing lead location, echo‐defined target segments, and CRT response. Results: Registration time (264 ± 25 seconds) and accuracy (4.3 ± 2.3 mm) were found clinically acceptable. A good agreement between pacing location and echo‐suggested segments was found in 20 (out of 21) CRT responders. Perioperative integration of the proposed workflow was successfully tested in 2 patients. No additional radiation, compared with the existing workflow, was required. Conclusions: The fusion tool facilitates understanding of the spatial relationship between the coronary veins and the LV function and may help targeted LV lead delivery. [ABSTRACT FROM AUTHOR]

Rationale: Atrial fibrillation is associated with increased mortality as well as morbidity. There is strong evidence for an association between atrial fibrillation and sleep apnea. It is not known whether treatment of sleep apnea with continuous positive airway pressure (CPAP) will reduce the burden of atrial fibrillation.Objective: The Treatment of Sleep Apnea in Patients with Paroxysmal Atrial Fibrillation study will investigate the effects of CPAP in patients with paroxysmal atrial fibrillation and sleep apnea.Design: The trial has a dual center, randomized, controlled, open-label, parallel design.Methods: Two centers will enroll a total of 100 patients with both paroxysmal atrial fibrillation and sleep apnea (apnea-hypopnea index [AHI] ≥ 15 events/h) who are scheduled for catheter ablation. Patients will be randomized in a 1:1 ratio to CPAP or control group (50 patients in each arm). The effects of CPAP treatment on atrial fibrillation will be determined using an implanted loop recorder (Reveal LINQ™, Medtronic) that detects all arrhythmia episodes. The primary endpoint is a reduction of the total burden of atrial fibrillation in the intervention group, after 5 months' follow-up (preablation). Reduction in the arrhythmia recurrence rate after ablation is the main secondary endpoint. All patients will be followed up for 12 months after ablation.Conclusion: This study is the first randomized controlled trial that will provide data on the effects of CPAP therapy in patients with paroxysmal atrial fibrillation and sleep apnea. The results are expected to improve our understanding of the interaction between paroxysmal atrial fibrillation and sleep apnea. ClinicalTrials.gov Identifier. NCT02727192. [ABSTRACT FROM AUTHOR]

Objectives: This study sought to examine the relationship between proximal aortic dilation and systemic vascular function in men with bicuspid aortic valve (BAV). Background: Proximal aortic dilation in subjects with BAV is associated with structural and functional abnormalities in the ascending aorta. Methods: We studied 32 men (median age 31 years [range 28 to 32 years]) with nonstenotic BAV categorized into 2 subgroups according to proximal ascending aorta dimensions (nondilated ≤35 mm and dilated ≥40 mm, respectively). Sixteen healthy men were studied as control subjects. Flow-mediated dilation in response to hyperemia (a marker of endothelial dysfunction) and carotid–femoral pulse wave velocity (an index of aortic stiffness) were assessed, and peripheral blood was sampled for matrix metalloproteinases (MMP-2 and -9) and their tissue inhibitors (TIMP-1 and -2), respectively. Cardiac chamber and aortic dimensions were assessed by echocardiography and cardiac magnetic resonance imaging, respectively. Results: Despite the similar severity of aortic stenosis, left ventricular mass, and function, men with dilated aortas had blunted brachial flow-mediated vasodilation to hyperemia (5% [interquartile range (IQR) 4% to 6%] vs. 8% [IQR 7% to 9%] change, p = 0.001), higher carotid–femoral pulse wave velocity (9.3 cm/s [IQR 9 to 10 cm/s] vs. 7 cm/s [IQR 6.9 to 7.4 cm/s], p = 0.001), and significantly higher plasma levels of MMP-2 (1,523 [IQR 1,460 to 1,674] vs. 1,036 [IQR 962 to 1,167], p = 0.001) compared with men with BAV and nondilated aorta. Values for MMP-9, TIMP-1 and -2 levels, and nitroglycerin-induced (endothelium-independent) vasodilation were similar in all 3 groups. Conclusions: Young men with BAV and dilated proximal aortas manifest systemic endothelial dysfunction, increased carotid–femoral pulse wave velocity, and higher plasma levels of MMP-2. These observations could introduce new targets for screening and perhaps for therapeutic intervention. [Copyright &y& Elsevier]

Objectives: The objective of this study was to investigate whether strain Doppler echocardiography performed immediately after revascularization by percutaneous coronary intervention could predict the extent of myocardial scar, determined by contrast-enhanced magnetic resonance imaging (MRI). Background: There is considerable variability in survival rate after percutaneous coronary intervention, and accurate early risk stratification is therefore of major clinical importance. Methods: Thirty individuals with acute anterior myocardial infarction were examined with longitudinal strain by Doppler 1.5 h after revascularization. The extent of scarring 9 months later was analyzed by MRI in 16 corresponding myocardial segments. Strain in all left ventricular segments was averaged to obtain a global value. Infarct size was estimated by clinical parameters and cardiac markers. Results: A good correlation was found between the global strain and total infarct size (R = 0.77, p < 0.00001). A multivariate regression analysis showed that global peak strain and serum glutamic oxaloacetic transaminase correlated with the infarct size measured by MRI (p = 0.0001 and p = 0.001, respectively). Furthermore, a clear inverse relationship was found between the segmental strain and the transmural extent of infarction in each segment (R = 0.67, p < 0.0001). Conclusions: This study demonstrates that assessment of regional and global strain at 1.5 h after reperfusion therapy correlates with size and transmural extent of myocardial infarction as determined by contrast-enhanced MRI. The novel global strain parameter is a valuable predictor of the total extent of myocardial infarction and may therefore be an important clinical tool for risk stratification in the acute phase of myocardial infarction. [Copyright &y& Elsevier]

Objectives: The aim of the study was to compare the ability of the tissue Doppler echocardiographic imaging (TDI) modalities velocity, strain, and displacement to quantify systolic myocardial function. Background: Several TDI modalities may be used to quantify regional myocardial function, but it is not clear how the different modalities should be applied. Methods: In 10 anesthetized dogs we measured left ventricular pressure, longitudinal myocardial velocity, strain, and displacement by TDI at baseline and during left anterior descending coronary artery (LAD) stenosis and occlusion. Reference methods were segmental shortening by sonomicrometry and segmental work. In 10 patients with acute anterior wall infarction (LAD occlusion) and 15 control subjects, velocity, strain, and displacement measurements were performed. Results: In the animal study, systolic strain correlated well with segmental shortening (r = 0.96, p < 0.01) and work (r = 0.90, p < 0.01), and differentiated well between non-ischemic (−13.5 ± 3.2% [mean ± SD]), moderately ischemic (−6.5 ± 2.8%), and severely ischemic myocardium (7.1 ± 13.2%). The ratio post-systolic strain/total strain also differentiated well between levels of ischemia. Displacement and ejection velocity had weaker correlations with segmental shortening (r = 0.92 and r = 0.74, respectively) and regional work (r = 0.85 and r = 0.69), and there was marked overlap between values at baseline and at different levels of ischemia. In the human study, systolic strain differentiated well between infarcted and normal myocardium (1.0 ± 5.0% vs. −17.8 ± 3.8%), whereas systolic displacement (−0.3 ± 1.3 mm vs. −2.3 ± 0.6 mm) and ejection velocity (0.9 ± 0.6 cm/s vs. 2.2 ± 0.6 cm/s) showed overlap. In the infarction group, strain was reduced in segments with infarcted tissue, while systolic velocity and displacement were reduced in all segments and did not reflect the extension of the infarct. Conclusions: Strain was superior to velocity and displacement for quantification of regional myocardial function. Provided technical limitations can be solved, strain Doppler is the preferred TDI modality for assessing function in ischemic myocardium. [Copyright &y& Elsevier]

Objectives: The aim of this study was to validate speckle tracking echocardiography (STE) as a method for angle-independent measurement of regional myocardial strain, using sonomicrometry and magnetic resonance imaging (MRI) tagging as reference methods. Background: Tissue Doppler imaging allows non-invasive measurement of myocardial strain in the left ventricle (LV), but is limited by angle dependency. Methods: Strain measurements with STE were obtained by a custom-made program that allowed tracking of two-dimensional motion of speckle patterns in a B-mode image. In anesthetized dogs, we compared LV long- and short-axis measurements by STE to sonomicrometry during preload changes and regional myocardial ischemia. Measurements in the two orthogonal axes were obtained simultaneously in a single imaging plane. In human subjects, long-axis strain by STE and MRI tagging were compared in multiple segments of the LV. Results: In the experimental study there was good correlation and agreement between STE and sonomicrometry for systolic strain in the long axis (r = 0.90, p < 0.001; 95% limits of agreement −4.4% to 5.0%) and systolic shortening in the short axis (r = 0.79, p < 0.001; −5.6% to 5.1%). In the clinical study, 80% of the segments could be analyzed, and correlation and agreement between STE and MRI tagging were good (r = 0.87, p < 0.001; −9.1% to 8.0%). Conclusions: Speckle tracking echocardiography provides accurate and angle-independent measurements of LV dimensions and strains and has potential to become a clinical bedside tool for quantifying myocardial strain. [Copyright &y& Elsevier]

Aims: We aimed to characterize the substrate of T-wave inversion (TWI) using cardiac magnetic resonance (CMR) and the association between diffuse fibrosis and ventricular arrhythmias (VA) in patients with mitral valve prolapse (MVP)., Methods and Results: TWI was defined as negative T-wave ≥0.1 mV in ≥2 adjacent ECG leads. Diffuse myocardial fibrosis was assessed by T1 relaxation time and extracellular volume (ECV) fraction by T1-mapping CMR. We included 162 patients with MVP (58% females, age 50 ± 16 years), of which 16 (10%) patients had severe VA (aborted cardiac arrest or sustained ventricular tachycardia). TWI was found in 34 (21%) patients. Risk of severe VA increased with increasing number of ECG leads displaying TWI [OR 1.91, 95% CI (1.04-3.52), P = 0.04]. The number of ECG leads displaying TWI increased with increasing lateral ECV (26 ± 3% for TWI 0-1leads, 28 ± 4% for TWI 2leads, 29 ± 5% for TWI ≥3leads, P = 0.04). Patients with VA (sustained and non-sustained ventricular tachycardia) had increased lateral T1 (P = 0.004), also in the absence of late gadolinium enhancement (LGE) (P = 0.008)., Conclusions: Greater number of ECG leads with TWI reflected a higher arrhythmic risk and higher degree of lateral diffuse fibrosis by CMR. Lateral diffuse fibrosis was associated with VA, also in the absence of LGE. These results suggest that TWI may reflect diffuse myocardial fibrosis associated with VA in patients with MVP. T1-mapping CMR may help risk stratification for VA., (© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Aims: We aimed to assess sex-specific phenotypes and disease progression, and their relation to exercise, in arrhythmogenic cardiomyopathy (AC) patients., Methods and Results: In this longitudinal cohort study, we included consecutive patients with AC from a referral centre. We performed echocardiography at baseline and repeatedly during follow-up. Patients' exercise dose at inclusion was expressed as metabolic equivalents of task (MET)-h/week. Ventricular arrhythmia (VA) was defined as aborted cardiac arrest, sustained ventricular tachycardia, or appropriate therapy by implantable cardioverter-defibrillator. We included 190 AC patients (45% female, 51% probands, age 41 ± 17 years). Ventricular arrhythmia had occurred at inclusion or occurred during follow-up in 85 patients (33% of females vs. 55% of males, P = 0.002). Exercise doses were higher in males compared with females [25 (interquartile range, IQR 14-51) vs. 12 (IQR 7-22) MET-h/week, P < 0.001]. Male sex was a marker of proband status [odds ratio (OR) 2.6, 95% confidence interval (CI) 1.4-5.0, P = 0.003] and a marker of VA (OR 2.6, 95% CI 1.4-5.0, P = 0.003), but not when adjusted for exercise dose and age (adjusted OR 1.8, 95% CI 0.9-3.6, P = 0.12 and 1.5, 95% CI 0.7-3.1, P = 0.30, by 5 MET-h/week increments). In all, 167 (88%) patients had ≥2 echocardiographic examinations during 6.9 (IQR 4.7-9.8) years of follow-up. We observed no sex differences in deterioration of right or left ventricular dimensions and functions., Conclusion: Male AC patients were more often probands and had higher prevalence of VA than female patients, but not when adjusting for exercise dose. Importantly, disease progression was similar between male and female patients., (© The Author(s) 2021. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Background: Acceleration of the mitral ring during isovolumic contraction has been proposed as a load-independent index of global left ventricular (LV) contractility. This study investigates whether myocardial isovolumic acceleration (IVA) reflects regional contractility., Methods and Results: In acutely instrumented, anesthetized dogs, we measured LV pressure, myocardial long-axis velocities, and IVA by tissue Doppler imaging (TDI) and sonomicrometry at different levels of global LV contractility and preload and during regional myocardial ischemia (reduced flow in the left anterior descending coronary artery). Dobutamine caused dose-dependent increments in IVA from 3.6+/-0.6 (mean+/-SEM) to a maximum of 7.1+/-1.4 m/s2 (P<0.01) by TDI, and there were parallel increments in LV dP/dt(max) (P<0.01). However, volume loading decreased IVA from 3.6+/-0.6 to 2.5+/-0.4 m/s2 (P<0.05), whereas LV dP/dt(max) was unchanged, and LV pressure-segment length loop analysis confirmed unchanged regional contractility. During myocardial ischemia, sonomicrometry indicated severely depressed regional function, whereas IVA remained unchanged. These findings were confirmed when IVA was measured by sonomicrometry. In contrast to peak ejection velocity that increased from apex toward the LV base, peak IVC velocity was maximum midway between apex and base. The onset of IVA coincided with onset of the first heart sound by phonocardiography. Peak IVA occurred at a LV pressure of 14+/-1 mm Hg, ie, close to end-diastole., Conclusions: There was no consistent relationship between peak IVA and regional myocardial contractility. Peak IVA was markedly load dependent and did not reflect impaired myocardial function during ischemia. Peak IVA may reflect late-diastolic events and possibly wall oscillations that are related to global LV function. Peak IVA seems to have limited potential in the assessment of regional myocardial function.