Marco J.W. Götte

Interventricular Mechanical Asynchrony in Pulmonary Arterial Hypertension Left-to-Right Delay in Peak Shortening Is Related to Right Ventricular Overload and Left Ventricular Underfilling

OBJECTIVES The purpose of this study was to explore in pulmonary arterial hypertension (PAH) whether the cause of interventricular asynchrony lies in onset of shortening or duration of shortening. BACKGROUND In PAH, leftward ventricular septal bowing (LVSB) is probably caused by a left-to-right (L-R) delay in myocardial shortening. METHODS In 21 PAH patients (mean pulmonary arterial pressure 55 +/- 13 mm Hg and electrocardiogram-QRS width 100 +/- 16 ms), magnetic resonance imaging myocardial tagging (14 ms temporal resolution) was applied. For the left ventricular (LV) free wall, septum, and right ventricular (RV) free wall, the onset time (T(onset)) and peak time (T(peak)) of circumferential shortening were calculated. The RV wall tension was estimated by the Laplace law. RESULTS The T(onset) was 51 +/- 23 ms, 65 +/- 4 ms, and 52 +/- 22 ms for LV, septum, and RV, respectively. The T(peak) was 293 +/- 58 ms, 267 +/- 22 ms, and 387 +/- 50 ms for LV, septum, and RV, respectively. Maximum LVSB was at 395 +/- 45 ms, coinciding with septal overstretch and RV T(peak). The L-R delay in T(onset) was -1 +/- 16 ms (p = 0.84), and the L-R delay in T(peak) was 94 +/- 41 ms (p < 0.001). The L-R delay in T(peak) was not related to the QRS width but was associated with RV wall tension (p < 0.05). The L-R delay in T(peak) correlated with leftward septal curvature (p < 0.05) and correlated negatively with LV end-diastolic volume (p < 0.05) and stroke volume (p < 0.05). CONCLUSIONS In PAH, the L-R delay in myocardial peak shortening is caused by lengthening of the duration of RV shortening. This L-R delay is related to LVSB, decreased LV filling, and decreased stroke volume.

Quantification of regional contractile function after infarction: strain analysis superior to wall thickening analysis in discriminating infarct from remote myocardium

OBJECTIVES Using two-dimensional wall thickening (WT) (expressed as percentage) and strain analysis, regional contractile myocardial function was quantified and compared in 13 control subjects and 13 patients with a first myocardial infarction (MI). The findings in the patient group were related to global ventricular function and infarct size. BACKGROUND In patients with coronary artery disease, regions with dysfunctional myocardium cannot be differentiated easily from regions with normal function by planar WT analysis. Physiologic factors, in combination with limitations of conventional imaging techniques, affect the calculation of WT. Quantitative assessment of contractile function by magnetic resonance (MR) tissue tagging and strain analysis may be less affected by these factors. METHODS Two-dimensional regional WT and strain were calculated in three short-axis MR cine and tagged images, respectively. Left ventricular volumes and ejection fraction (EF) were obtained from a series of contiguous short-axis cine images. RESULTS In patients with infarct-related ventricles, WT and strain analysis both revealed reduced myocardial function, as compared with control subjects (p < 0.005 and p < 0.001, respectively). However, WT analysis yielded no significant regional differences in function between infarct-related and remote myocardium (p = 0.064), whereas strain analysis did (p < 0.005). For detecting dysfunctional myocardium of electrocardiographically and angiographically defined infarct areas, WT analysis had a sensitivity of 69% and a specificity of 92%, whereas strain analysis demonstrated a sensitivity of 92% and a specificity of 99%. The EF correlated with WT (r = 0.76, p < 0.005) and strain (r = 0.89, p < 0.001). CONCLUSIONS Two-dimensional strain analysis is more accurate than planar WT analysis in discriminating dysfunctional from functional myocardium, and it provides a strong correlation between regional myocardial and global ventricular function.

Early Onset and Progression of Left Ventricular Remodeling After Alcohol Septal Ablation in Hypertrophic Obstructive Cardiomyopathy

Background—Alcohol septal ablation (ASA) reduces left ventricular outflow tract (LVOT) pressure gradient in patients with hypertrophic obstructive cardiomyopathy (HOCM), which leads to left ventricular remodeling. We sought to describe the early to midterm changes and modulating factors of the remodeling process using cardiac MRI (CMR). Methods and Results—CMR was performed at baseline and 1 and 6 months after ASA in 29 patients with HOCM (age 52±16 years). Contrast-enhanced CMR showed no infarct-related hyperenhancement outside the target septal area. Septal mass decreased from 75±23 g at baseline to 68±22 and 58±19 g (P<0.001) at 1- and 6-month follow-up, respectively. Remote, nonseptal mass decreased from 141±41 to 132±40 and 111±27 g (P<0.001), respectively. Analysis of temporal trends revealed that septal mass reduction was positively associated with contrast-enhanced infarct size and transmural or left-sided septal infarct location at both 1 and 6 months. Remote mass reduction was associated with infarct location at 6 months but not with contrast-enhanced infarct size. By linear regression analysis, percentage remote mass reduction correlated significantly with LVOT gradient reduction at 6-month follow-up (P=0.03). Conclusions—Left ventricular remodeling after ASA occurs early and progresses on midterm follow-up, modulated by CMR infarct size and location. Remote mass reduction is associated with infarct location and correlates with reduction of the LVOT pressure gradient. Thus, myocardial hypertrophy in HOCM is, at least in part, afterload dependent and reversible and is not exclusively caused by the genetic disorder.

Left ventricular torsion: an expanding role in the analysis of myocardial dysfunction.

During left ventricular (LV) torsion, the base rotates in an overall clockwise direction and the apex rotates in a counterclockwise direction when viewed from apex to base. LV torsion is followed by rapid untwisting, which contributes to ventricular filling. Because LV torsion is directly related to fiber orientation, it might depict subclinical abnormalities in heart function. Recently, ultrasound speckle tracking was introduced for quantification of LV torsion. This fast, widely available technique may contribute to a more rapid introduction of LV torsion as a clinical tool for detection of myocardial dysfunction. However, knowledge of the exact function and structure of the heart is fundamental for understanding the value of LV torsion. LV torsion has been investigated with different measurement methods during the past 2 decades, using cardiac magnetic resonance as the gold standard. The results obtained over the years are helpful for developing a standardized method to quantify LV torsion and have facilitated the interpretation and value of LV torsion before it can be used as a clinical tool.

Quantification of global left ventricular function : Comparison of multidetector computed tomography and magnetic resonance imaging. A meta-analysis and review of the current literature

Cardiac morbidity and mortality are closely related to cardiac volumes and global left ventricular (LV) function, expressed as left ventricular ejection fraction. Accurate assessment of these parameters is required for the prediction of prognosis in individual patients as well as in entire cohorts. The current standard of reference for left ventricular function is analysis by short-axis magnetic resonance imaging. In recent years, major extensive technological improvements have been achieved in computed tomography. The most marked development has been the introduction of the multidetector CT (MDCT), which has significantly improved temporal and spatial resolutions. In order to assess the current status of MDCT for analysis of LV function, the current available literature on this subject was reviewed. The data presented in this review indicate that the global left ventricular functional parameters measured by contemporary multi-detector row systems combined with adequate reconstruction algorithms and post-processing tools show a narrow diagnostic window and are interchangeable with those obtained by MRI.

Coronary microvascular resistance: methods for its quantification in humans

Coronary microvascular dysfunction is a topic that has recently gained considerable interest in the medical community owing to the growing awareness that microvascular dysfunction occurs in a number of myocardial disease states and has important prognostic implications. With this growing awareness, comes the desire to accurately assess the functional capacity of the coronary microcirculation for diagnostic purposes as well as to monitor the effects of therapeutic interventions that are targeted at reversing the extent of coronary microvascular dysfunction. Measurements of coronary microvascular resistance play a pivotal role in achieving that goal and several invasive and noninvasive methods have been developed for its quantification. This review is intended to provide an update pertaining to the methodology of these different imaging techniques, including the discussion of their strengths and weaknesses.

The influence of through-plane motion on left ventricular volumes measured by magnetic resonance imaging: implications for image acquisition and analysis.

In the evaluation of the left ventricular (LV) function using magnetic resonance imaging (MRI), a stack of parallel short-axis (SA) cine images is acquired that covers the whole LV. The aim of this study is to quantify the contribution to the LV volume parameters, provided by the most basal image plane that shows the LV wall only in end diastole (ED) but not in end systole (ES). In 57 healthy volunteers (31 men, mean body surface area 1.87 m2), a complete set of parallel SA images was acquired (10-mm slice distance) by breathhold segmented k-space cine MRI (7 ky lines per beat). The LV end-diastolic volume (EDV), stroke volume (SV), ejection fraction (EF), and cardiac output (CO) were determined by slice summation. Calculations were performed both with and without inclusion of the most basal slice. With inclusion of the most basal slice, all parameters were significantly (p < 0.001) larger compared with the values obtained by excluding this slice. EDV was 134 +/- 29 ml versus 113 +/- 26 ml; SV was 93 +/- 18 ml versus 72 +/- 16 ml; EF was 70 +/- 4% versus 64 +/- 4%; and CO was 5.3 +/- 1.4 l/min versus 4.1 +/- 1.1 l/min. The inclusion of the most basal slice leads to significantly larger values of LV volume parameters. Thus, this most basal SA image slice should be included in calculating the EDV. Whether or not this basal SA slice also contributes to the ES volume should be decided by using anatomical criteria on the ES image. The projection line onto the ES image of a long-axis view provides an additional criterion.

MRI-derived left ventricular function parameters and mass in healthy young adults: Relation with gender and body size

Purpose: To obtain normal values of left ventricular (LV) end-diastolic volume (EDV), stroke volume (SV), cardiac output (CO) and LV mass, in relation to gender, weight (W), length (L) and body surface area (BSA). Methods: Sixty-one healthy volunteers (32 male, 22.4 ± 2.2 years) were examined, weight was 70.9 ± 12.2 kg, length was 1.78 ± 0.09 m, BSA was 1.88 ± 0.19 m2. Segmented k-space breathhold cine MRI was used to obtain a stack of parallel short-axis images, from which LV volumes and end-diastolic mass were derived by slice summation. Four different body size indices were studied: W, L, L2 and BSA. Results: After indexing for L, L2 and BSA, the gender differences in all LV parameters are still persisting. After indexing for W, gender differences persist for EDV and EDM, but are no longer observed for SV and CO. Separate regression analyses for males and females were performed. EDV, SV, CO and EDM correlated significantly with each body size index, both in males and in females. L or BSA were in general better predictors for LV parameters than W. Linear regression equations of EDV (ml) vs. L(m) were for males: EDV = 275 × L − 359 and for females: EDV = 190 × L − 215. Equations of SV(ml) vs. L were for males: SV = 186 × L − 237 and for females: SV = 118 × L − 121. Equations of LV mass(g) vs. L were for males: Mass = 175 × L − 179 and for females: Mass = 65.8 × L − 10.9. Conclusion: Most gender differences in LV parameters remain even after correction for body size indices. Normal reference values for LV parameters are given in relation to body size indices, by calculating regression coefficients separately for males and females. These normal values serve to obtain more accurate reference values for a patient with given gender, weight and length, and thus to improve the differentiation between normal and abnormal LV parameters.

Three-Dimensional Myocardial Strains at End-Systole and During Diastole in the Left Ventricle of Normal Humans

This paper presents the three-dimensional strains in the normal human left ventricle (LV) at end-systole and during diastole. Magnetic resonance tissue tagging was used to measure strain in the left-ventricular heart wall in 10 healthy volunteers aged between 28 and 61 years. The three-dimensional motion was calculated from the displacement of marker points in short- and long-axis cine images, with a time resolution of 30 msec. Homogeneous strain analysis of small tetrahedrons was used to calculate deformation in 18 regions of the LV over a time span of 300 msec starting at end systole. End-systolic radial strain was largest near the heart base, and circumferential and longitudinal strains were largest near the apex. During diastole, the circumferential-longitudinal shear strain (associated with LV torsion) was found to recover earlier than the axial strains. Assessment of three-dimensional diastolic strain is possible with MR tagging. Comparison of patient strain against normal strain may permit early detection of regional diastolic dysfunction.

Cardiac dysfunction after aneurysmal subarachnoid hemorrhage: Relationship with outcome

Objective: To assess whether cardiac abnormalities after aneurysmal subarachnoid hemorrhage (aSAH) are associated with delayed cerebral ischemia (DCI) and clinical outcome, independent from known clinical risk factors for these outcomes. Methods: In a prospective, multicenter cohort study, we performed echocardiography and ECG and measured biochemical markers for myocardial damage in patients with aSAH. Outcomes were DCI, death, and poor clinical outcome (death or dependency for activities of daily living) at 3 months. With multivariable Poisson regression analysis, we calculated risk ratios (RRs) with corresponding 95% confidence intervals. We used survival analysis to assess cumulative percentage of death in patients with and without echocardiographic wall motion abnormalities (WMAs). Results: We included 301 patients with a mean age of 57 years; 70% were women. A wall motion score index ≥1.2 had an adjusted RR of 1.2 (0.9–1.6) for DCI, 1.9 (1.1–3.3) for death, and 1.8 (1.1–3.0) for poor outcome. Midventricular WMAs had adjusted RRs of 1.1 (0.8–1.4) for DCI, 2.3 (1.4–3.8) for death, and 2.2 (1.4–3.5) for poor outcome. For apical WMAs, adjusted RRs were 1.3 (1.1–1.7) for DCI, 1.5 (0.8–2.7) for death, and 1.4 (0.8–2.5) for poor outcome. Elevated troponin T levels, ST-segment changes, and low voltage on the admission ECGs had a univariable association with death but were not independent predictors for outcome. Conclusion: WMAs are independent risk factors for clinical outcome after aSAH. This relation is partly explained by a higher risk of DCI. Further study should aim at treatment strategies for these aSAH-related cardiac abnormalities to improve clinical outcome.