Increased Left Ventricular Wall Thickness Research Articles

Prognostic significance of left ventricular concentric remodelling in patients with aortic stenosis

Four patterns of left ventricular (LV) geometry (normal, concentric remodelling, concentric hypertrophy and eccentric hypertrophy) have been described in aortic stenosis (AS). Although LV concentric remodelling (LVCR), characterized by normal LV mass despite increased LV wall thickness, is frequently observed in AS, its prognostic implication has been not specifically studied. We aimed to assess, using echocardiography, the prognostic implication of LVCR in asymptomatic or minimally symptomatic patients with AS. Overall, 331patients (mean age 73±13years; 45% women) with AS (aortic valve area≤1.3cm2) and an ejection fraction >50% were enrolled. The endpoints were mortality with conservative management and mortality with conservative and/or surgical management. Sixty-three (19%) patients died under conservative management (follow-up 29±1months). The highest risk of mortality under conservative management compared with patients with normal LV geometry was observed for LVCR (adjusted hazard ratio [HR]: 3.53, 95% confidence interval [CI]: 1.19-10.46; P=0.023), followed by concentric LVH (adjusted HR: 2.97, 95% CI: 1.02-8.60; P=0.045). Aortic valve replacement was performed in 96patients (29%) during the entire follow-up (37±1months); 72 (22%) patients died. Only LVCR remained independently associated with an increased risk of mortality when surgical management during the entire follow-up was considered (adjusted HR: 2.93, 95% CI: 1.19-7.23; P=0.020). Among the patterns of LV geometry in AS, LVCR portends the worst outcome. Patients with LVCR and AS have a considerable increased risk of mortality, regardless of clinical management.

First Reported Case of Khat Cardiomyopathy and Malignant Hypertension in Australia

A 37 year old Eritrean migrant presented to our hospital with cardiac failure and malignant hypertension on a background of heavy khat consumption. He had additional cardiac risk factors of morbid obesity and cigarette smoking. There was no other medical history and he took no regular medications. Echocardiography demonstrated a dilated cardiomyopathy with severe biventricular systolic dysfunction (LV ejection fraction 25%) and moderate functional mitral regurgitation. Coronary angiography revealed normal coronary arteries but confirmed severe global left ventricular dysfunction. Our patient commenced appropriate anti-hypertensive and heart failure therapy. Follow-up cardiac MRI within two months of khat cessation demonstrated near-complete recovery, with ejection fraction 48%, mild LV dilation, mildly increased LV wall thickness, and no late gadolinium enhancement to suggest established fibrosis. Khat (Catha edulis) is a leaf with amphetamine-type properties cultivated in East Africa and the Arabian Peninsula since the 7th century. It is estimated there are 20 million users of khat worldwide, with khat-chewing traditionally restricted to men. Documented adverse health effects include psychosis, peptic ulcer disease, hepatitis, cardiomyopathy, accelerated coronary artery disease and malignant hypertension. With increasing migration, khat-related health problems are likely to become more prevalent in Australian healthcare settings. This case underlines the need for doctors caring for East African patients, particularly males, to enquire as to khat consumption as part of comprehensive health screening.

Abstract 455: FGF23-induced Cardiac Hypertrophy is Reversible

Left ventricular hypertrophy (LVH) is a common feature of cardiovascular disease in chronic kidney disease (CKD) and affects up to 90% of patients by the time they reach dialysis. Serum levels of fibroblast growth factor (FGF) 23 continuously rise as patients progress to renal failure. We have previously shown that FGF23 can activate FGF receptor (FGFR) 4 and the PLCgamma/calcineurin/NFAT signaling cascade in cardiac myocytes and induce hypertrophy in vitro and in vivo. Administration of an isoform-specific FGFR4 blocking antibody in the 5/6 nephrectomy rat model of CKD immediately after surgery protects rats from developing LVH, and delivery of a pan-FGFR blocker in CKD rats two weeks after surgery reverses LVH. To further study the reversibility of cardiac FGF23 effects, we elevated serum FGF23 levels in mice by administration of a high phosphate (2%) diet for three months. Animals developed LVH, as evident by significantly increased LV wall thickness and myocyte cross sectional area. When mice were switch from high phosphate to normal chow, the LVH phenotype resolved and cardiac parameters were comparable to those of mice that constantly received a normal diet. Furthermore, isolated cardiac myocytes recovered within 24 hours from FGF23-induced hypertrophy upon removal of FGF23. Finally, the FGFR4 blocking antibody was capable of reversing FGF23-induced hypertrophy in vitro. Our data indicate that FGF23-induced LVH is reversible and treatable. Interfering with FGF23/FGFR4 signaling in the heart might provide a novel therapeutic strategy to tackle cardiac injury in CKD. We propose that progression and reversibility of cardiac injury might depend on the duration of cardiac FGF23/FGFR4 activation.

Athletic Cardiac Remodeling in US Professional Basketball Players.

The incidence of sudden cardiac death is higher in US basketball players compared with other athlete groups. However, the recognition of the risk for sudden cardiac death among basketball players is challenging because little is known regarding athletic cardiac remodeling in these athletes or athletes of similarly increased size. To perform a comprehensive cardiac structural analysis of National Basketball Association (NBA) professional athletes. Echocardiographic observational study of NBA players on the active rosters for the 2013-2014 and 2014-2015 seasons was performed from December 16, 2013, to December 12, 2014. The policy of the NBA mandates annual preseason stress echocardiograms for each player. The NBA has sanctioned Columbia University Medical Center to conduct annual health and safety reviews of these echocardiograms. Data were analyzed from January to May 2015. Cardiac variables assessed included left ventricular (LV) size, mass, wall thickness, and hypertrophy patterns and function; left atrial volume; and aortic root diameter. All dimensions were biometrically scaled. Of the 526 athletes included in the study, 406 (77.2%) were African American and 107 (20.3%) were white, with a mean (SD) age of 25.7 (4.3) years. Mean (SD) athlete height was 200.2 (8.8) cm; mean body surface area, 2.38 (0.19) m2. Left ventricular size and mass in NBA athletes were proportional to body size, extending to the uppermost biometrics of the cohort. Left ventricular hypertrophy was present in 144 athletes (27.4%). African American athletes had increased LV wall thickness (unadjusted mean, 11.2 mm; 95% CI, 11.1-11.3 mm) and LV mass (unadjusted mean, 106.3 g/m2; 95% CI, 104.6-108.0 g/m2) compared with LV wall thickness (unadjusted mean, 10.5 mm; 95% CI, 10.3-10.7 mm; P < .001) and LV mass (unadjusted mean, 102.2 g/m2; 95% CI, 99.0-105.4 g/m2; P = .029) in white athletes. The maximal aortic root diameter in the cohort was 42 mm. Aortic root diameters reached a plateau at the uppermost biometric variables. Five athletes (1.0%) had an LV ejection fraction of less than 50%, and all ventricles augmented normally with exercise. This study provides normative cardiac data for a group of athletes with greater anthropometry than any previously studied athlete group and for a group known to have elevated rates of sudden cardiac death. These data can be incorporated into clinical assessments for the primary prevention of cardiac emergencies in basketball players and the athletic community at large.

Cardiologic Phenotypes and Natural History of FAC

Fifty years ago, the focus on the Val30Met type of the disease, in which neurologic manifestations predominate, led to the widespread notion that hereditary transthyretin-related amyloidosis (ATTR) was essentially a neurologic disease. It is now clear that ATTR is extremely heterogeneous on both genotypic and phenotypic grounds. The clinical spectrum of the disease ranges from an almost exclusive neurologic involvement to strictly cardiac manifestations. This heterogeneity is linked to several factors including specific transthyretin mutations, geographic distribution and endemic vs. non-endemic aggregation type. The existence of exclusively or predominantly cardiac phenotypes makes the recognition of the disease very challenging since it can mimic other more common causes of left ventricular “hypertrophy”. Assessment of such patients should include an active search for possible red flags that can indicate the correct final diagnosis. More in general the clinician must be aware that: • Cardiac amyloidosis (CA) should be suspected in any patient with heart failure, unexplained increased LV wall thickness and non-increased end systolic left ventricular volume • In a patient with an initial diagnosis of hypertrophic cardiomyopathy (HCM), look for the infiltrative phenotype hidden beneath the hypertrophic one! • A distinctive sign of CA is the abnormal ratio between left ventricular thickness and QRS voltages rather than low QRS voltages, alone. The absence of low QRS voltages doesn’t rule out a CA if the context is otherwise fitting and up to 20% of subjects with CA can have electrocardiographic evidence of left ventricular hypertrophy. • In an elderly man with unexplained concentric left ventricular hypertrophy, especially in the absence of hypertension, always consider the possibility of wtTTR CA! • Amyloidotic cardiomyopathy in an elderly patient with monoclonal gammopathy is not necessarily related to AL: consider the possibility of wTTR + MGUS • Longitudinal LV function can be severely depressed despite a normal LVEF and the myocardial contraction fraction is often low suggesting reduced global myocardial shortening. • Myocardial deformation is reduced in amyloidotic cardiomiopathy but the apex is generally spared • In CA, Gadolinium distribution at MRI is heterogeneous: subendocardial late gadolinium enhancement (LGE) is not the only diagnostic pattern and the absence of LGE does not exclude CA. • Bilateral carpal tunnel syndrome in a man with HCM-like phenotype on echo is highly suggestive of TTR-related CA The natural history of ATTR is only partially known, due to the rarity of the disease and its high genotypic heterogeneity. Patients with ATTR cardiomyopathy have a much more indolent course than those with AL etiology. Progression of neurological disease and heart failure are the leading causes of death. As in AL amyloidosis, in ATTR the presence of cardiac involvement is an incremental risk factor for overall and cardiovascular events. Consequently, non-Val30Met mutations, in which cardiac involvement is more frequent and severe, appear to be associated with a particularly poor prognosis, even after successful OLT . Very little is known about the underlying cause and the incidence of sudden death, which has been reported to be associated with the occurrence of advanced atrioventricular blocks, ventricular tachycardia/fibrillation, or, probably more frequently, electromechanical dissociation.

Left ventricular structural and functional abnormalities in dogs with hyperadrenocorticism

ObjectivesHyperadrenocorticism has been reported to cause left ventricular (LV) structural and functional abnormalities in human patients. The purpose of the present study was to assess the incidence and features of LV structural and functional changes in dogs with hyperadrenocorticism. AnimalsTwenty-two client-owned dogs with pituitary-dependent hyperadrenocorticism (n = 15) and cortisol-secreting adrenocortical tumors (n = 7) and 6 control dogs were enrolled in this study. MethodsEchocardiographic examinations were performed and non-invasive measurements of systolic blood pressure (SBP) were obtained. ResultsThe normalized LV wall thickness and LV mass index of the affected dogs differed significantly from those of control dogs. Using a published reference value for M-mode measurements, 15 of the 22 dogs (68%) were found to have increased LV wall thickness. Eleven of the 15 (73%) dogs with increased LV wall thickness were normotensive, and no significant correlation between LV wall thickness and SBP was found. ConclusionsRegardless of the presence of systemic hypertension, hyperadrenocorticism should be included in the differential diagnosis of underlying disorders that may cause LV hypertrophy in dogs.

Short-Term Caloric Restriction Suppresses Cardiac Oxidative Stress and Hypertrophy Caused by Chronic Pressure Overload

BackgroundCaloric restriction (CR) prevents senescent changes, in which reactive oxygen species (ROS) have a critical role. Left ventricular (LV) hypertrophy is a risk factor for cardiovascular diseases. We examined whether CR alters cardiac redox state and hypertrophy from chronic pressure overload. Methods and ResultsMale c57BL6 mice were subjected to ascending aortic constriction (AAC) with ad libitum caloric intake (AL + AAC group) or 40% restricted caloric intake (CR + AAC group). CR was initiated 2 weeks before AAC and was continued for 4 weeks. Two weeks after constriction, AAC increased LV wall thickness, impaired transmitral flow velocity, and augmented myocyte hypertrophy and fibrosis, in association with enhancement of BNP and collagen III expressions in the AL + AAC group. In the AL + AAC group, oxidative stress in cardiac tissue and mitochondria were enhanced, and NADPH oxidase activity and mitochondrial ROS production were elevated. These changes were significantly attenuated in the CR + AAC group. Additionally, in antioxidant systems, myocardial glutathione peroxidase and superoxide dismutase activities were enhanced in the CR + AAC group. ConclusionsChronic pressure overload increased cardiac oxidative damage, in association with cardiac hypertrophy and fibrosis. Short-term CR suppressed oxidative stress and improved cardiac function, suggesting that short-term CR could be a useful strategy to prevent pressure overload–induced cardiac injury.

Abstract 185: Using the Platelet Proteome to Identify Novel Biomarkers in Heart Failure With Preserved Ejection Fraction

Introduction: The platelet proteome is an untapped resource for identifying novel proteins that may reflect a disease process. The platelet proteome is understudied in heart failure. We hypothesize that the platelet proteome will change composition in patients with heart failure with ejection fraction (HFpEF). Using mass-spectral analysis, we examined the platelet proteome from subjects with heart failure with preserved ejection fraction (HFpEF) to identify proteins associated with the disease process. Methods/Results: We conducted a case-controlled prospective study in which we drew blood samples from hospitalized subjects with symptoms of HFpEF (n=9), the same subjects several weeks later without symptoms (n=7) and control subjects (n=8). The subjects with HFpEF were older and had a higher incidence of atrial fibrillation and smoking compared to the control group. There were no significant differences in body mass index, and history of hypertension, hyperlipidemia, coronary artery disease or diabetes. The HFpEF group had increased LV wall thickness, left atrial volume, and diastolic dysfunction. Mass spectrometry of the platelet rich abstract obtained from the blood samples of the 3 groups identified 6,102 proteins with 5 scans with peptide probabilities of ≥0.85. Of the 6,102 proteins, 165 were present only in symptomatic subjects, 78 were only found in asymptomatic subjects and 157 proteins were unique to the control group. S100A8 and its receptor, CD36 were two proteins identified consistently in HFpEF samples when compared with controls. Using ELISA, we further confirmed that plasma S100A8 levels were increased in subjects with HFpEF (728±358) vs. control (314±154). Conclusion: Platelets may harbor proteins associated with HFpEF. S100A8 is present in the platelets of subjects with HFpEF and increased in the plasma of the same subjects. S100A8 has been linked with other cardiovascular disease such as atherosclerosis and risk for myocardial infarction, stroke, or death. This is the first report on the association between S100A8 and HFpEF.

Echocardiographic assessment of the cardiac amyloidoses.

Cardiac amyloidosis is a cardiomyopathy characterized by increased left ventricular (LV) wall thickness and normal or decreased LV cavity size. Congestive heart failure in cardiac amyloidosis is generally considered a predominantly diastolic phenomenon, with systolic dysfunction only occurring in late-stage disease. Echocardiography is a noninvasive, reproducible method of assessing cardiac features and function in cardiac amyloidosis, and some echocardiographic indices are prognostic for the amyloidoses, with M-mode and 2-dimensional echocardiography able to detect increased LV wall thickness. Moreover, Doppler flow measurements can incrementally assess diastolic LV dysfunction, which is characteristic of cardiac amyloidosis, and provide important prognostic information. Additionally, tissue Doppler imaging can detect subtle changes in both systolic and diastolic LV function, which cannot be detected by Doppler flow measurements, and LV longitudinal strain assessed by color tissue Doppler and speckle tracking echocardiography can provide more accurate LV functional and prognostic information than tissue Doppler imaging. This review describes the advances in echocardiography and its crucial role in the diagnosis and management of cardiac amyloidosis.

Abstract 19687: Morphological and Clinical Characteristics of Late and Young Age Onset Apical Hypertrophic Cardiomyopathy: Insight from a 13-Year Registry of Hypertrophic Cardomyopathy

Background: Apical hypertrophic cardiomyopathy (ApHCM) might have different morphological and clinical features according to the age of disease onset, probably result from the distinct mechanism of pathogenesis. The aim of this study was to evaluated the morphological and clinical differences according to the age of disease onset in patients with ApHCM. Methods: This was a retrospective, observational study of 56 ApHCM patients (31 males, mean 65±9 years). Among 426 patients with diagnosed ApHCM from 2000 until 2013, we selected 56 patients who met the inclusion criteria: [[Unable to Display Character: &amp;#9332;]] patiens who diagnosed with ApHCM before 60 years old and current age &gt;60 years old, (group A, early onset, n=16); and [[Unable to Display Character: &amp;#9333;]] who diagnosed with ApHCM after 60 years old who had no evidence of apical hypertrophy confirmed by previous echocardiography (group B, late onset, n=40). Morphological LV feature was assessed by transthoracic echocardiography, which were divided into pure and mixed type. Furthermore, hemodynamic parameters and clinical events were also evaluated. Results: There were no differences in the presence of hypertension, LV systolic function and left atrial volume index between group A and B. However, early onset group A had more increased maximal wall thickness of LV apex (17.08±2.02 vs 15.43±1.68mm, p=0.005), and more incidence of pure type (100% (16/16) vs 56.8% (21/40), p=0.001) compare than late onset group B. Group B had older age (65±5 vs 72±4 years, p=0.001), increased LV end-diastolic dimension (51.25±2.32 vs 48.58±3.37mm, p=0.006), increased E/E’ (11.24±2.94 vs 14.60±6.37, p=0.049) with decreased E’ (5.61±1.34 vs 4.66±1.38cm/s, p=0.024) respectively.There were no significant differences in the risk of cardiovascular complication such as atrial fibrillation and stoke between group A and B. Conclusions: There was obvious different clinical characteristics according to the age of disease onset. Early onset ApHCM has typical morphological feature and relatively preserved LV diastolic function, compared with late onset ApHCM. Our result supports that late onset ApHCM was related to decreased LV diastolic function and increased LV wall thickness, which reflects the potential myocardial remodeling with aging.

Abstract 18297: Clinical and Prognostic Utility of Cardiac Magnetic Resonance Imaging in Multiple Myeloma Patients With Suspected Amyloidosis

Background: Upto 30% of patients with multiple myeloma have AL amyloidosis and cardiac involvement is associated with worse outcomes in these patients. Traditional screening modalities including EKG, echocardiography and biomarkers have limited value. The aim of this study was to evaluate the role of “screening” cardiac MRI in a large multiple myeloma population at a large specialized referral center. Methods &amp; Results: 164 consecutive patients with multiple myeloma who underwent cardiac MRI between 6/2005 and 10/2011 were enrolled in this study. Primary endpoint was all cause death. Clinical, EKG, echocardiographic, biomarker and MRI predictors for death were analyzed. Mean age of population was 63+10 years, 40% females and 16% African Americans. 30% of the population had MRI evidence of cardiac involvement. There were 26 patients who had biopsy proven systemic amyloidosis, of whom 62% showed cardiac involvement on MRI. 81% patients with confirmed cardiac amyloidosis on endomyocardial biopsy had typical MR pattern of cardiac involvement. During a median follow up period of 702 days (mean 1019 (950) days), there were 59 deaths (36%). Amyloid pattern on cardiac MRI (OR 2.19), elevated BNP and increased LV wall thickness on MRI were significant predictors of mortality . (All p&lt;0.05) Conclusions: This is the largest study to date evaluating the role of cardiac MRI in multiple myeloma patients with suspected cardiac amyloidosis. Cardiac MRI is a clinically robust tool for risk stratification of this subset of patients.

Left Ventricular Hypertrophy in a Runner

A 63-year-old male runner presented for outpatient cardiology evaluation of decreased exercise tolerance and increased left ventricular (LV) wall thickness noted on an echocardiogram obtained by his primary care provider. The patient had been an avid runner since a young age; however, over the previous months he had noted decreased exercise tolerance prompting evaluation by his primary physician. His medical history was only significant for hypertension that had been well controlled with a single medication. ECG revealed sinus bradycardia with markedly elevated voltage in the anterolateral precordial leads (Figure 1). Echocardiography with strain imaging demonstrated increased LV wall thickness measuring 1.8 cm at the basal septum and 1.7 cm at the basal inferolateral wall (Figure 2A). Ejection fraction was noted to be normal; however, longitudinal strain imaging was markedly abnormal throughout the septum, extending into adjacent regions of the anterior and inferior walls and normalizing in the lateral wall and apex (Figure 2B and 2C). Figure 1. ECG demonstrating sinus bradycardia with increased voltage throughout the anterolateral precordial leads. Figure 2. A , Two-dimensional …

Cardiac magnetic resonance evaluation of left ventricular remodelling distribution in cardiac amyloidosis

BackgroundCardiac amyloidosis (CA) is associated with typical morphological features on echocardiography, including concentric LV hypertrophy (LVH). Cardiac magnetic resonance (CMR) can accurately depict anatomy in different cardiomyopathies. Our aim was...

Glucagon-like peptide-1 receptor agonists for diabetes mellitus: a role in cardiovascular disease.

Diabetes mellitus, defined as a fasting plasma glucose of ≥126 mg/dL or a glycosylated hemoglobin A1c level (HbA1c) of ≥6.5%, afflicts ≈12.9% of adults in the United States and nearly 285 million adults worldwide.1,2 Diabetes mellitus is a major risk factor for the development of cardiovascular disease, independently conferring a 2-fold excess risk of coronary heart disease and stroke.3 Macrovascular events in diabetes mellitus remain the leading cause of mortality, and the burden of cardiovascular disease attributable to diabetes mellitus has increased over the past decade.4 An increase in the prevalence of obesity has contributed to the rise in diabetes mellitus. Additionally, obesity independently increases the risk of cardiovascular disease in patients with diabetes mellitus.5 Although strict glycemic control unequivocally reduces the microvascular complications of diabetes mellitus, the macrovascular benefits of intensive therapy have been difficult to establish, with conflicting results from large clinical trials.6–9 Multifactorial strategies are recommended to reduce cardiovascular risk in diabetes mellitus through enhanced glycemic control, blood pressure reduction, lipid management, weight loss, and physical activity.10 Unfortunately, despite aggressive interventions for hyperglycemia, <50% of patients achieve standard HbA1c targets with conventional therapy.11 Polypharmacy is required to achieve glycemic control in the majority of patients within 3 years of diagnosis.12 Although combinations of drug classes can synergistically target multiple pathophysiological defects, novel therapies are required to manage diabetes mellitus and mitigate cardiovascular risks. Dipeptidyl-peptidase IV (DPP-IV) inhibitor and glucagon-like peptide-1 (GLP-1) receptor agonist incretin therapies were developed to complement conventional treatment options for diabetes mellitus. Despite promising initial reports of cardioprotective effects, DPP-IV inhibitors have failed to demonstrate improved cardiovascular outcomes in large clinical trials.13–15 Randomized studies to evaluate cardiovascular outcomes associated with GLP-1 receptor agonists are currently underway. This review presents …

123 Comprehensive Cardiovascular MRI for the non-invasive Assessment of Patients with Systemic Hypertension

BackgroundHypertensive disease is a major risk factor for cardiovascular morbidity and mortality. Cardiovascular MRI not only provides a non-invasive method for the assessment of potential secondary causes of hypertension (including...

Echocardiographic Study of Cardiac Structure in Cyclists and Runners

We sought to study the cardiac morphology of cyclists and runners in male and female athletes and control subjects and to find association cardiac morphological measurements with body composition measurements. Endurance training is associated with increases in both left ventricular mass (LVM) and left ventricular end-diastolic dimension (LVEDD). Cardiac morphology shows sports specific adaptations which are studied in the two groups, runners involving lower limb and cyclists involving upper limb. 28 runners and 26 cyclists were taken to do a comparison study with 38 control subjects, aged between 18-25 years of age and comprising of males and females both. All participants underwent transthoracic echocardiography and hydrostatic underwater weighing for body composition along with routine measurements. Athletes showed enlarged LV dimensions and mass (p<0.05) as compared to controls. Right ventricular and aortic root dimensions were also found to be significantly higher in athletes (p<0.05). Lean tissue mass was found to be independent predictor of LVM. Increased LV wall thickness in relation to the ventricular dimension appears to be proportionate in runners; it is disproportionate in cyclists, probably because of the isometric training component involved during upper limb training cycling. Hence runners show eccentric hypertrophy and cyclist showed mixed eccentric and concentric hypertrophy. LVM was found to be correlated only to lean tissue mass. The extent of LV remodeling (athletic heart) in trained individuals may reflect a normal physiologic response to increased lean tissue mass induced by training.

HEART's Original [症例] 拡張不全による左心不全にて発症した正常壁厚心アミロイドーシスの1例

HEART's Original [症例] 拡張不全による左心不全にて発症した正常壁厚心アミロイドーシスの1例

What is the role of cardiac MRI in the diagnosis of left ventricular non-compaction?

Background The prevalence of left ventricular non-compaction is not well established. Using 2-D echocardiography, less than 1% of patients are diagnosed with this entity. Using cardiac MRI, approximately 3% of patients have evidence of LV non-compaction. This variance may be related to the difference in spatial resolution between these 2 imaging techniques. Using a large institutional cardiac imaging database, 2-D echo and cardiac MRI results were compared in patients with LV non-compaction. Methods Of 1,255 patients in our cardiac imaging database, 38 patients (3%) with a diagnosis of LV non-compaction were identified. Twenty-two of these 38 patients had undergone both 2-D echo and cardiac MRI exams. The reported diagnoses with each imaging modality were tabulated, along with measurements of left ventricular antero-septal and infero-posterior wall thickness for both modalities. The 2-D echo and cardiac MRI wall thickness dimensions were statistically compared using a paired sample t-test. Results All 38 patients had a diagnosis of LV non-compaction on cardiac MRI, using criteria of non-compacted/compacted myocardium > 2.5 to 1.0 and deep LV trabeculations. None of the 22 patients with both 2-D echo and cardiac MRI exams had a diagnosis of LV non-compaction on their 2-D echo study. However, 15 of 22 patients (68%) had a diagnosis of LVH on their 2-D echo study, while only 3 had LVH on their cardiac MRI study. The mean ASWT on 2-D echo was 1.38 cm, while the mean ASWT on cMRI was 1.16 cm (p<0.005). The mean IPWT on 2-D echo was 1.31 cm, while the IPWT on cMRI was only 0.89 cm (p<0.001). Conclusions These data suggest that LV non-compaction, identifiable on cardiac MRI, is frequently diagnosed as LVH on 2-D echo. This discrepancy appears to be explained by the statistically significant difference in both antero-septal and infero-posterior LV wall thickness measurements between the 2 imaging modalities. It is suspected that this difference is related to the inferior spatial resolution of 2-D echo relative to cMRI. On the basis of these data, patients with LVH on 2-D echo should be considered for a cardiac MRI exam to determine if the increased LV wall thickness is truly LVH or an undiagnosed LV non-compaction cardiomyopathy.

Assessing the Athlete’s Heart

The initial report of the athlete’s heart dates back to the late 1890s. The concept that endurance-based exercise and strength-based exercise lead to distinctly different changes in left ventricular (LV) structure was proposed in the 1970s and has been confirmed by more recent studies. Advances in cardiac imaging, particularly echocardiography and cardiac magnetic resonance imaging, have allowed for more precise characterization of the structural changes that develop in the hearts of athletes engaged in different sporting disciplines. Despite our improved understanding of exercise-induced cardiac remodeling, the findings of: 1) increased LV chamber dimension, 2) increased LV wall thickness, and 3) increased right ventricular (RV) chamber dimension continue to be accompanied by significant diagnostic uncertainty in clinical practice. Determining whether these entities arise from exercise-induced cardiac remodeling or represent pathologic cardiomyopathy requires the integration of a number of diagnostic techniques, including evaluations with echocardiography and/or cardiac magnetic resonance imaging. Ambiguous cases require additional testing, such as cardiopulmonary exercise testing and assessing the response to a period of prescribed detraining. Novel imaging techniques coupled with physiologic provocation that assess regional LV and RV function may make the distinction between physiologic adaptation and pathology more clear in the future.

Left ventricular chamber dimensions and wall thickness by cardiovascular magnetic resonance: comparison with transthoracic echocardiography

Cardiovascular magnetic resonance (CMR) is a reference standard imaging technique in assessment of cardiomyopathies due to the accurate measurement of cardiac volumes and mass. In clinical routine, transthoracic echocardiography (TTE) is the standard first-line technique and is commonly used for follow-up. In this study we examined how CMR-derived measurement of left ventricular (LV) chamber dimensions and wall thickness correspond to TTE. A total of 101 subjects underwent TTE and CMR (men, n = 67, mean age 62 ± 9 years) and formed a normal group (n = 44), a group with dilated LV cavity (n = 33; LV internal dimensions in end-diastole ≥ 52 mm) and a group with increased LV wall thickness (n = 24; interventricular septum ≥ 12 mm, inferolateral wall both in end-diastole ≥ 12 mm). Standard TTE measurements of LV chamber and wall thickness were compared to CMR-derived values in the basal short-axis slice and the 3-chamber (3-CH) view. Interstudy reproducibility for CMR was done in 23 subjects. In all groups, there was a better agreement between TTE and 3-CH for all dimensions. The intraobserver and interobserver agreements were superior for 3-CH view. In addition, both CMR approaches showed sound interstudy reproducibility for all dimensions and in all groups. We demonstrate a good agreement between CMR and TTE in LV chamber dimension and wall thickness measurements. We propose that with CMR using a 3-CH approach is superior in reproducibility and closer in concordance with TTE-derived values.