Cardiac changes in subclinical and overt hyperthyroid women: retrospective study

ObjectiveLonger QRS duration on the ECG is associated with increased cardiovascular (CV) mortality. To evaluate potential mechanisms, we examined in this study the relationship between QRS duration and left ventricular...

Several coronary angiographic studies have reported that enlarged and tortuous epicardial coronary arteries are characteristic of patients with left ventricular concentric hypertrophy (LVCH). Recently, we showed that small volumes opacified by contrast medium can be accurately measured by 64-multislice computed tomography (MSCT) and that there is a direct relationship between the coronary artery volume and left ventricular (LV) mass. However, the relationship of coronary artery volume with LV mass in patients with dilated cardiomyopathy (DCM) is unknown. The present study was designed to investigate this issue. Thirteen patients with DCM and 18 patients with LVCH who underwent MSCT angiography were included in this analysis. The coronary arteries were segmented on a workstation, and the appropriate window settings obtained from the results of the phantom experiments were applied to the volume-rendered images to calculate the total coronary artery volume (right and left coronary arteries). The absolute coronary lengths and volumes in patients with LVCH and DCM were greater than those in controls. The coronary artery volumes adjusted for LV mass in patients with DCM were found to be smaller than those in patients with LVCH or in controls, and these values did not differ between patients with LVCH and controls (DCM 4.1 ± 0.9, LVCH 5.4 ± 1.4, controls 5.5 ± 2.3 ml/100 g of LV mass, P < 0.005; DCM vs LVCH, P < 0.01; and DCM vs control, P < 0.0005). This study showed that the increase in the coronary artery volume in patients with LVCH matched the increase in LV mass, but a decreased coronary volume with regard to LV mass was characteristic of patients with DCM.

Pericardial fat has been implicated in the pathogenesis of obesity-related cardiovascular disease. Whether the associations of pericardial fat and measures of cardiac structure and function are independent of the systemic effects of obesity and visceral adiposity has not been fully explored. Participants from the Framingham Heart Study (n=997; 54.4% women) underwent chest and abdominal computed tomography and cardiovascular magnetic resonance imaging between 2002 and 2005. Pericardial fat, intrathoracic fat, and visceral adipose tissue quantified from multidetector computed tomography, along with body mass index and waist circumference, were examined in relation to cardiovascular magnetic resonance measures of left ventricular (LV) mass, LV end-diastolic volume, and left atrial dimension. In women, pericardial fat (r=0.20 to 0.35, P<0.001), intrathoracic fat (r=0.25 to 0.37, P<0.001), visceral adipose tissue (r=0.24 to 0.45, P<0.001), body mass index (r=0.36 to 0.53, P<0.001), and waist circumference (r=0.30 to 0.48, P<0.001) were directly correlated with LV mass, LV end-diastolic volume, and left atrial dimension. In men, pericardial fat (r=0.19 to 0.37, P<0.001), intrathoracic fat (r=0.17 to 0.31, P<0.001), visceral adipose tissue (r=0.19 to 0.36, P<0.001), body mass index (r=0.32 to 0.44, P<0.001), and waist circumference (r=0.34 to 0.44, P<0.001) were directly correlated with LV mass and left atrial dimension, but LV end-diastolic volume was not consistently associated with adiposity measures. Associations persisted after multivariable adjustment but not after additional adjustment for body weight and visceral adipose tissue, except for pericardial fat and left atrial dimension in men. Pericardial fat is correlated with cardiovascular magnetic resonance measures, but the association is not independent of or stronger than other ectopic fat stores or proxy measures of visceral adiposity. An important exception is left atrial dimension in men. These results suggest that the systemic effects of obesity on cardiac structure and function may outweigh the local pathogenic effects of pericardial fat.

Left ventricular (LV) function and mass were measured in six conscious dogs at weekly intervals during the progression of tachycardia-induced dilated cardiomyopathy (DCM) and during a 1-mo recovery period from DCM (post-DCM). LV end-diastolic volume and LV wall stress increased and LV ejection fraction decreased with each week of pacing. Despite the increased LV wall stress, LV mass did not change during the progression of tachycardia DCM. One week post-DCM resulted in an improved LV ejection fraction and normalization of neurohormonal profiles. However, 1 wk post-DCM was accompanied by a 26% increase in LV mass and persistent LV chamber dilation. Isolated myocyte function was examined and compared with that in six normal control dogs. Myocyte percent and myocyte velocity of shortening were 19 and 32% lower, respectively, in the post-DCM group compared with controls. Thus termination of the tachycardia subsequent to the development of DCM resulted in persistent LV chamber dilation and abnormalities in myocyte contractile function. The improved LV pump function with early recovery from tachycardia-induced DCM was mediated by LV hypertrophy and a subsequent reduction in LV wall stress rather than a normalization of LV geometry and myocyte contractile function.

Introduction: Obesity is associated with excess cardiovascular morbidity and mortality as well as structural and functional differences in left ventricular (LV) mass (LVM), end-diastolic volume (LVEDV), and stroke volume despite indexation. Hypothesis: We hypothesize that overweight and obesity impact LV structure and function in a healthy community dwelling cohort. Methods: Framingham Offspring study participants (N=678, 62%F; 65±9y) free of any history of hypertension, myocardial infarction, heart failure, or CMR wall-motion abnormality and underwent bSSFP CMR at 1.5T. They were stratified by sex and body mass index (BMI) category (normal weight =18.5 to 24.9; overweight =25.0 to 29.9; obese ≥30 kg/m 2 ). LVM was measured from contiguous short-axis images, then indexed to height (HT, m), body surface area (BSA, m 2 ), and weight (WT, kg). We calculated myocardial contraction fraction (MCF), a marker of LV myocardial shortening, as LV stroke volume divided by LV myocardial volume. The ratio of LVM/LVEDV was used as a measure of LV concentricity to evaluate LV structure. Results: The Table shows MCF, LV concentricity, and indexed LVM (LVMi) stratified by BMI. WT-indexation resulted in a declining LVMi with increasing BMI in both men and women. However, indexation to HT showed an increasing LVMi with higher BMI. BSA-indexation remained consistent across BMI categories in both men and women. MCF decreased and concentricity increased with increasing BMI in both sexes. Conclusion: The association of LVMi with BMI varies by indexation method. In a healthy, community-dwelling cohort, BSA yields “consistent” LVM indexation across BMI categories. However, MCF decreased, and concentricity increased with increasing categories of BMI. These adverse alterations of MCF and concentricity may provide insight into obesity-related LV remodeling, whereas consideration of LVM alone may not. These data lay the groundwork for further outcomes analyses in this population.

Echocardiographic assessment of left ventricular hypertrophy: Comparison to necropsy findings

Fetal cardiac examination is an important part of fetal malformation screening. The purposes of this study were to describe the left ventricular (LV) mass in the second and third trimesters by 2-dimensional echocardiography using area-length calculation methods and to examine the clinical usefulness of this procedure in evaluation of gestational age (GA)- and fetal weight-related LV mass changes. Five hundred healthy fetuses were divided into 2 groups (250 participants per group): second- and third-trimester groups. The estimated fetal weight (EFW) was computed according to the Hadlock formula (Radiology 1984; 150:535-540). The LV mass at end diastole (LVd mass) and LV mass at end systole (LVs mass) were measured, and the difference between the LVd mass and LVs mass [LV(d-s) mass], LVd mass/EFW ratio, and LVs mass/EFW ratio were calculated. The EFW, LVd mass, LVs mass, and LV(d-s) mass were all significantly greater in the third-trimester group than the second-trimester group (P < .05), whereas the LVd mass/EFW and LVs mass/EFW ratios did not differ between the groups (P > .05). The LVd mass, LVs mass, and LV(d-s) mass all significantly correlated with GA and weight (P< .001), but the LVd mass/EFW and LVs mass/EFW ratios did not (P > .05). Two-dimensional echocardiography using area-length calculation methods can effectively provide measurements for LV mass and can sensitively indicate fetal weight- and GA -related changes in LV mass. Fetal cardiac mass measurement is a useful parameter for evaluation of fetal heart development.

There is current controversy on the association between subclinical hyperthyroidism and hypertension. Data from cohort studies have not been available yet. The present study was designed to longitudinally investigate possible associations of subclinical hyperthyroidism with blood pressure, pulse pressure and the risk of hypertension. We used data from the population-based, prospective cohort Study of Health in Pomerania and included 2910 subjects (1469 women) aged 20-79 years with completed 5-year examination follow-up. Subjects with increased serum TSH levels or overt hyperthyroidism were excluded. Serum TSH levels below 0.25 mIU/l with free triiodothyronine and free thyroxine levels within the reference range were defined as subclinical hyperthyroidism. Blood pressure was measured according to standard methods. Multivariable analyses adjusted for age, sex, overweight, obesity, smoking status and time between the examinations did not reveal any statistically significant association between subclinical hyperthyroidism and any of the blood pressure-related variables in the whole study population. Although the 5-year hypertension incidence was higher in subjects with subclinical hyperthyroidism compared with those without (31.4 vs 19.2%; risk ratio 1.64; 95% confidence interval (CI) 1.17-2.28, P=0.006), both groups did not differ with respect to the risk of hypertension, after analyses were adjusted for confounders (relative risk 1.23, 95% CI 0.91-1.68, P=0.182). Analyses yielded similar results in subjects without thyroid disease and in those who took no antihypertensive medication. Subclinical hyperthyroidism is not associated with changes in blood pressure, pulse pressure or incident hypertension.

The aim of this study was to investigate the relations of left ventricular (LV) mass and geometry to LV function in patients with predialysis chronic kidney disease (CKD), by real-time 3-dimensional echocardiography (RT3-DE). Echocardiography was performed on 76 consecutively enrolled patients (51 men) with different stages of CKD, including 26 patients with mild CKD (CKD stages 1-2) and 50 patients with moderate-to-severe CKD (CKD stages 3-5). LV mass and LV end-diastolic volume were measured by RT3-DE. Greater prevalence of LV diastolic dysfunction and higher mitral E/myocardial velocities in early diastole (Em) values were noted in patients with moderate-to-severe CKD. In the moderate-to-severe CKD group, patients with increased LV mass had lower myocardial velocities in peak systole (Sm) and longer isovolumic relaxation time (IVRT). In the mild CKD group, patients with increased LV mass to volume ratios had lower Em. Moderate-to-severe CKD was associated with lower Sm and Em and higher mitral rapid filling to Em (E/Em) ratios by LV mass quartile stratification. Using LV mass/volume quartile stratification, moderate-to-severe CKD was associated with longer IVRT, lower Sm and higher mitral E/Em. Multivariable logistic regression analysis showed that CKD severity was the most independent predictor of elevated LV filling pressure (odds ratio = 2.96, p=0.019). Increased LV mass impaired LV contraction and relaxation in patients with moderate-to-severe CKD. Concentric remodeling impaired LV diastolic function in patients with mild CKD. CKD severity was positively associated with elevated LV filling pressure.

In chronic uremia, cardiomyopathy manifests itself as systolic dysfunction, concentric left ventricular (LV) hypertrophy, or LV dilatation. To determine the impact of renal transplantation on uremic cardiomyopathy, all dialysis patients participating in a long-term cohort study who received a successful renal transplant were followed with echocardiography. The transplanted group comprised 102 of 433 (24%) endstage renal disease (ESRD) patients. They were significantly younger and, on starting ESRD therapy, had significantly less ischemic heart disease and cardiac failure than the overall ESRD cohort. During followup, ischemic heart disease developed in only 1 patient and none experienced cardiac failure. In the 12% (n = 12) of patients with systolic dysfunction before renal transplant, fractional shortening normalized in all patients, increasing from 21.5 +/- 4.6% to 33.5 +/- 5.6% after transplantation. In the 41% (n = 41) with concentric LV hypertrophy before transplantation, the LV mass index improved from 158 +/- 39 g/m2 to 132 +/- 39 g/m2. LV dilatation was present in 32% (n = 32) of patients before transplantation. After transplantation, LV volume fell from 116 +/- 3.1 ml/m2 to 89 +/- 21 ml/m2, and LV mass index in this group fell from 166 +/- 55 g/m2 to 135 +/- 37 g/m2. It was not possible to associate risk factors characteristic of the uremic state with the improvement in cardiac structure and function, although the fall in LV mass was significantly associated with fall in blood pressure. We conclude that correction of the uremic state by renal transplantation leads to normalization of LV contractility in systolic dysfunction, regression of hypertrophy in concentric LV hypertrophy, and improvement of cavity volume in LV dilatation. The degree of improvement suggests that dialysis patients with uremic cardiomyopathy would benefit from renal transplantation.

Left ventricular geometry and adverse cardiovascular events in chronic hemodialysis patients on prolonged therapy with ACE inhibitors

A clinical and therapeutic approach to thyrotoxicosis with thyroid-stimulating hormone suppression only

Objectives — Structural changes in the extracranial carotid artery are associated with an increase in left ventricular (LV) mass and relative wall thickness. The present study was performed to determine the relation of LV mass index and relative wall thickness to suspected atherosclerotic steno-occlusive disease of the intracranial arteries on magnetic resonance angiography (MRA) in noncardioembolic ischaemic stroke patients.Methods — We retrospectively analysed the records of acute ischaemic stroke patients who underwent echocardiography and intracranial MRA. Patients with potential sources of cardioembolism, or known causes of vascular steno-occlusive disease including dissection, vasculitis, and moyamoya disease, were excluded from the study. LV mass indexes and relative wall thicknesses were estimated using echocardiography. Patients were divided into four groups according to their LV mass index and relative wall thickness: concentric LV hypertrophy, eccentric LV hypertrophy, concentric LV remodelling, and normal geometry. MRA was used to evaluate steno-occlusive disease in the basilar artery (BA) and the horizontal portion of the middle cerebral artery.Results — A total of 212 patients were included, and logistic regression analysis revealed that BA steno-occlusive disease was related to LV relative wall thickness, but not LV mass index.The prevalence of BA disease was significantly higher in the concentric LV hypertrophy group than in the normal geometry group. Steno-occlusive disease of the middle cerebral artery was not closely related to the structural changes in the left ventricle.Conclusion — Increased LV relative wall thickness may be an independent risk factor for BA steno-occlusive disease or may share pathogenic mechanisms with BA disease.

Hypertrophic cardiomyopathy (HCM) is a common monogenetic cardiac disease with a prevalence of 0.2%1 that usually is inherited as an autosomal dominant trait with variable penetrance and expression. Clinically, HCM is defined by the presence of left ventricular (LV) hypertrophy (LVH) unexplained by abnormal loading conditions.1 The natural history varies from an asymptomatic course to drug-refractory angina/dyspnea, sudden cardiac death (SCD), and end-stage heart failure. The incidence of HCM-related SCD is approximately 1% to 2% in children and adolescents and 0.5% to 1% in adults.2,3 In this review, we examine the impact of advanced diagnostic imaging technologies on HCM, with particular emphasis on the detection of particular genetic subtypes. In ≈60% of cases, HCM is inherited as an autosomal dominant trait caused by mutations in genes coding for cardiac sarcomere proteins (Figure 1).4–7 Mutations in genes encoding Z-disc proteins and proteins involved in calcium regulation account for <5% of cases. The absence of sarcomeric gene mutations can be explained by limitations of current mutation detection techniques or mutations in as yet unidentified genes, but in some cases, hypertrophy is caused by other diseases that mimic the phenotype of sarcomeric protein disease. Table 1 lists genetic disorders associated with HCM. Figure 1. A schematic illustration of a cardiac sarcomere. View this table: Table 1. Currently Known Genes Implicated in HCM More than 600 different sarcomeric gene mutations are reported in patients with HCM.8–16 The majority are missense mutations, but nonsense, frameshift, and in-frame insertion/deletion mutations also occur. Most mutations are characterized by incomplete penetrance and variable clinical expression likely due to locus heterogeneity and the effect of mutations at different locations within the same gene. Most mutations probably have a dominant negative effect on sarcomere function, but in some cases, haploinsufficiency (ie, only a single functional …

Background Data on changes in left atrial (LA) and left ventricular (LV) volumes after transcatheter mitral valve replacement (TMVR) are limited. Purpose This study sought to describe the anatomical and functional changes in left-sided cardiac chambers by computed tomography angiography (CTA) from baseline to 1-month after TMVR with Tendyne prosthesis. Methods We analyzed patients who underwent TMVR with Tendyne prosthesis (Abbott Structural, Menlo Park, CA) between 2015 and 2018. Changes in LV end-diastolic volume (LVEDV), ejection fraction (LVEF), mass (LV mass), LA volume and global longitudinal strain (GLS) were assessed at baseline and at 1-month after TMVR with CTA. Specific Tendyne implant characteristics were identified and correlated with remodeling changes. Results A total of 36 patients (mean age 73±8 years, 78% men, 86% secondary MR) were studied. There were significant decreases in LVEDV (268±68 vs. 240±66ml, p&amp;lt;0.001), LVEF (38±10 vs. 32±11%, p&amp;lt;0.001), LV mass (126±37 vs. 117±32g, p&amp;lt;0.001), LA volume (181±74 vs. 174±70 ml, p=0.027) and GLS (−12.6±5.1 vs. −9.5±4.0%, p&amp;lt;0.001) from baseline to 1-month follow-up. Favorable LVEDV reverse-remodeling occurred in the majority (30 of 36 patients, or 83%). Closer proximity of the Tendyne apical pad to the true apex was predictive of favorable remodeling (pad distance: 25.0±7.7 vs. 33.5±8.8mm, p=0.02 for those with and without favorable remodeling). Conclusions TMVR with Tendyne results in favorable left-sided chamber remodeling in the majority of patients treated, as detected on CTA at 1-month after implantation. CTA identifies the favorable post-TMVR changes, which could be related to specific characteristics of the device implantation. Funding Acknowledgement Type of funding source: None