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There is a known correlation between myocardial steatosis and heart function, but it is unclear how left ventricular diastolic function worsens over time in the myocardial steatosis setting. We sought to investigate whether intramyocardial fat deposition affects diastolic function over time. This was a retrospective analysis of patients who had undergone 1-3 echocardiography assessments between April 2011 and April 2017. Patients were divided into two groups: those with the presence of myocardial fat deposition in the left ventricular myocardium (assessed by having tissue within any 10-mm2 region with computed tomography values between - 190 and - 30 Hounsfield units; + MF), and those with absence of deposition not meeting the threshold (- MF). The rates of change of the standard early diastolic mitral annulus velocity (e') and the transmitral early peak velocity (E)/e' ratio at the second and third echocardiograph assessments were calculated relative to baseline. In total, 125 patients were eligible (+ MF, n = 39; - MF, n = 86) for inclusion. Compared with the - MF group, e' was significantly lower and E/e' was significantly higher in the + MF group at each scan timepoint, even when adjusted for body mass index and sex. A significant average decrease in e' and increase in E/e' was also observed in the + MF group across all scans compared with the - MF group. Myocardial steatosis was associated with an acceleration of decreased left ventricular diastolic function over time.

The safety and efficacy of intravenous insulin injection coupled with subsequent milk consumption was evaluated for high-quality cardiac viability F-18-fluorodeoxyglucose (18F-FDG) images. A total of 328 patients with known/suspected coronary artery disease received intravenous insulin injection with or without subsequent milk consumption for cardiac 18F-FDG imaging. When blood glucose levels had decreased by ≥ 20%, 18F-FDG was injected. Patients were scored for hypoglycemic symptoms using a 10-point scale (discomfort: 0, none; 1 to 3, mild; 4 to 6, moderate; 7 to 9, severe). An insulin-related hypoglycemic event was defined as an increased symptomatic score following insulin injection. The number of hypoglycemic events was significantly lower in the milk consumption group than in the group that did not (24/164 vs. 51/164, P

Isolated left ventricular noncompaction, where broad trabeculae and deep intertrabecular recesses are observed in the left ventricular myocardium resulting from an arrest in normal embryogenesis, is a rare cardiomyopathy. We present a report on isolated trabeculectomy and postoperative echocardiographic follow-up showing recovery of cardiac function for isolated left ventricular noncompaction.

Aim of the paper was to address all strengths and weakness of cardiac magnetic resonance (CMR) in arrhythmogenic cardiomyopathy, trying to highlight areas where further research and investigations should be carried out to fill current gaps in scientific knowledge. Arrhythmogenic cardiomyopathy represents a multifaceted clinical entity associated with arrhythmias and sudden death. Even though different diagnostic tools are available for appropriate identification and risk stratification, over the last few years cardiac magnetic resonance (CMR) has surfaced as an unmatched non-invasive imaging tool. CMR is mandatory in the evaluation of arrhythmogenic cardiomyopathy. It is the only imaging technique providing the identification of myocardial fibrosis, particularly for left ventricular myocardium, as recent evidences demonstrated that left ventricular involvement in arrhythmogenic cardiomyopathy is associated with greater risk of sudden death than lone right ventricular involvement.

BackgroundDuring left bundle branch (LBB) area pacing, it is important to confirm that the capture of the LBB is achieved, not just the capture of only the adjacent left ventricular myocardium (LV septal capture). Our aim was to establish ECG criteria for LBB capture by analyzing ECGs with confirmed LBB capture and non-capture. We hypothesized that since LBB pacing results in physiologic depolarization of the left ventricle then the native QRS can serve as a reference for the diagnosis of LBB capture in the same patient.MethodsOnly patients with direct evidence of LBB capture (output-dependent or refractoriness-dependent QRS morphology transition) were included. Several QRS characteristics were compared between the native rhythm and different types of LBB area capture. Receiver-operator characteristics analysis was performed to determine the optimal V6 R-wave peak time (RWPT) cut-off for LBB diagnosis.ResultsA total of 357 ECG tracing (124 patients) were analyzed: 118 with native rhythm, 124 with non-selective LBB capture, 69 with selective LBB capture and 46 with LV septal capture. Our hypotheses that during LBB capture the paced V6 RWPT (measured from QRS onset) equals the native V6 RWPT and that the paced V6 RWPT (measured from the stimulus) equals the LBB potential to V6 R-wave peak interval were positively validated. Criteria based on these rules had sensitivity and specificity of 98.0–88.2% and 85.7–95.4%, respectively. The optimal and 100% specific V6 RWPT values for differentiation between LBB capture and LV septal capture in patients with narrow QRS / right bundle branch block were 83 ms and 74 ms, respectively; while in patients with left bundle branch block/asystole/ventricular escape the optimal and 100% specific V6 RWPT values were 101 ms and 80 ms, respectively.ConclusionsNovel criteria for LBB capture were developed and optimal V6 RWPT cut-offs were determined.What this study addsWe showed that LBB pacing truly reproduce the physiological depolarization of the left ventricle since the paced V6 RWPT equals the native conduction V6 RWPT.Individualized LBB capture criteria, that use the native QRS as a reference, were developed.The optimal V6 RWPT values for differentiation between LBB capture and LV septal capture were determined, separately for patients with healthy and diseased LBB.

Introduction: 4D cardiac CT can reveal characteristics of arrhythmogenic right ventricular (RV) cardiomyopathy (ARVC) such as fat and fibrotic invasion into the RV and LV myocardium (RVM, LVM), an enlarged RV, reduced RV motion and bulging. Hypothesis: We could differentiate ARVC patients with fat and fibrotic invasion into the LVM from those without, using ECG, clinical, and other imaging characteristics. Methods: Retrospective analysis of 17 patients (11 males, 57±17 years) with suspected ARVC who underwent 4D cardiac CT. Results: 9 patients met the 2010 ARVC task force criteria. 4 had fat and fibrotic invasion into the LVM (group 1) but 5 did not (group 2). The remaining 8 did not fulfill the ARVC criteria (group 3). The proportion of males and age did not differ between groups. In groups 1, 2 and 3, respectively, 3 (75%), 4 (80%), and 1 (13%) patients had epsilon waves in V1-3 (group 1>3, P=0.033, group 2>3, P=0.005). 2 (50%), one (20%) and 4 (50%) had complete right bundle branch block (CRBBB) (all P=NS). Three (75%), 3 (60%), and 1 (13%) had inverted T waves in V1-3 or beyond (group 1>3, P=0.033). One (50%), 3 (75%), and 2 (50%) had terminal activation duration of QRS ≥55 ms measured from the nadir of the S wave to the end of the QRS, including R’, in V1, V2, or V3, in the absence of CRBBB (all P=NS). One (25%), 4 (80%) and 1 (13%) had sustained ventricular tachycardia (SVT; group 2>3, P=0.005). Two (50%), 1 (20%), and 3 (38%) had non-SVT (all P=NS). 4 (100%), 2 (40%), and 2 (25%) had clinical heart failure (group 1>2, P=0.019, group 1>3, P2, P=0.019, group 1>3, P3, P=0.002, group 2>3, P Conclusions: Most patients had RV enlargement on TTE and/or 4D CT. Presence of epsilon waves, reduced RV motion, and RV fat invasion on 4D CT may differentiate groups 1 and 2 from group 3, inverted T waves in V1-3 leads or beyond may differentiate group 1 from group 3, SVT may differentiate group 2 from group 3 but only clinical heart failure may differentiate groups 1 and 2.

Background: The adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) plays critical roles in regulating cellular growth and metabolism and is activated when cellular ATP levels decrease. The heterotrimeric structure of AMPK consists of a catalytic alpha (α) subunit and regulatory beta (β) and gamma (γ) subunits. The two isoforms of the catalytic α subunit have different cellular localization: AMPKα1 is predominantly found in the non-nuclear fraction and AMPKα2 is found in both the nuclear and the non-nuclear fractions. Both AMPKα isoforms reside in cardiomyocytes, increased expression of AMPKα1 during stress can trigger an increased inflammatory state whereas AMPKα2 has recently been recognized as a regulator of mitophagy, the selective degradation of damaged mitochondria by autophagy. Dysregulation in AMPKα1 and AMPKα2 has been reported in explanted failed human hearts. This study tested the hypothesis that mRNA and protein expression levels of AMPKα1 increase and that of AMPKα2 decrease in LV myocardium of dogs with chronic heart failure (HF) produced by microembolization. Methods: RNA was extracted and sodium dodecyl sulfate (SDS)-extract homogenate prepared from LV tissue of 6 dogs with microembolization-induced HF and 6 normal (NL) dogs. mRNA expression of AMPKα1 and AMPKα2 was measured using real-time PCR and normalized to GAPDH. Protein expression of AMPKα1 and AMPKα2 was measured by Western blotting and normalized to GAPDH. Bands were quantified in densitometric units (du). Results: mRNA and protein levels of GAPDH, used as internal control, were similar between NL and HF dogs. In HF dogs, mRNA expression of AMPKα2 was reduced by 5.09 fold and protein levels were reduced by 2.08 fold (1.02 ± 0.09 vs. 2.12 ± 0.18 du, p Conclusions: The results indicate that in LV myocardium of dogs with chronic HF, mRNA and protein levels for AMPKα1 are upregulated while AMPKα2 levels are downregulated compared to NL dogs. This AMPK isoform shift can trigger abnormalities of mitochondrial respiration and turnover that contribute to an abnormal energetic state characteristic of the failing heart.

This literature review in devoted to the potential of application of contrast-enhanced echocardiography (CEE) for assessment of structure and function of left cardiac chambers. It contains based on current recommendations discussion of main indications for CEE and analysis of its possibilities in evaluation of perfusion of the left ventricular myocardium, detection of myocardial ischemia, and assessment of myocardial viability. Data on CEE safety and possible side effects associated with the use of ultrasound contrasts are also presented.

Mitral regurgitation (MR) imposes left ventricular volume overload, triggering rapid ventricular dilatation, increased myocardial compliance, and, ultimately, cardiac dysfunction. Breakdown of the extracellular matrix has been hypothesized to drive these rapid changes, partially from an imbalance in the matrix metalloproteinases (MMPs) and their tissue inhibitors [tissue inhibitors of metalloproteinase (TIMPs)]. In the present study, we developed a rat model of severe MR that mimics the human condition and investigated the temporal changes in extracellular matrix-related genes, collagen biosynthesis proteins, and proteolytic enzymes over a 20-wk period. Male Sprague-Dawley rats were anesthetized to a surgical plane with mechanical ventilation, and a thoracotomy was performed to expose the apex. Using transesophageal ultrasound guidance, a needle was inserted into the beating heart to perforate the anterior mitral leaflet and create severe MR. Animals were survived for 20 wk, with some animals terminated at 2, 10, and 20 wk for analysis of left ventricular tissue. A sham group that underwent the same surgery without mitral leaflet perforation and MR were used as controls. At 2 wk post-MR, increased collagen gene expression was measured, but protein levels of collagen did not corroborate this finding. In parallel, MMP-1-to-TIMP-4, MMP-2-to-TIMP-1, and MMP-2-to-TIMP-3 ratios were significantly elevated, indicating a proteolytic milieu in the myocardium, possibly causing collagen degradation. By 20 wk, many of the initial differences seen in the proteolytic ratios were not observed, with an increase in collagen compared with the 2-wk time point. Altogether, this data indicates that an imbalance in the MMP-to-TIMP ratio may occur early and potentially contribute to the early dilatation and compliance observed structurally. NEW & NOTEWORTHY In this rodent model of severe mitral regurgitation that mimics the human condition, eccentric left ventricular dilatation occurred rapidly and persisted over the 20-wk period with parallel changes in myocardial collagen and matrix metalloproteinases that may drive the extracellular matrix breakdown.

Forward Projected Model-based Iterative Reconstruction SoluTion (FIRST) is a new reconstruction technique using CT, which provides successful reconstruction of high-quality CT images, especially in low contrast imaging. To evaluate improvements in the diagnostic accuracy of the detection of abnormal late enhancement (LE) in left-ventricular myocardium (LVM) using 320-slice CT with FIRST, we compared this modality with previous CT methods in patients with non-ischemic cardiomyopathy or a cardiac tumor.This was a retrospective study of 88 patients (56 males; 57 ± 15 years) suspected of having non-ischemic myocardial disease or a cardiac tumor. The first 52 consecutive patients (Group 1) underwent 16-slice CT at 140 kV tube voltage and an average tube current of 337 ± 20 mA, and 1.5 T MRI. The next 18 patients (Group 2) underwent 1st generation 320-slice CT at 120 kV tube voltage and an average tube current of 255 ± 106 mA, and 1.5T MRI; the remaining 18 patients (Group 3) underwent 2nd generation 320-slice CT with FIRST, at 80 kV tube voltage and a tube current of 800 mA, and 1.5T or 3T MRI.On patient-based analysis, no significant differences were observed between the 3 groups. For segment-based analysis, the specificity and overall accuracy were significantly higher (both P < 0.05) in Group 3 than in Group 1. Positive predictive value (PPV) was significantly higher in Group 3 than in Groups 1 and 2.The diagnostic accuracy of LE on CT for detecting myocardial fibrosis determined by late gadolinium-enhanced MRI was improved with the use of 2nd generation 320-slice CT with FIRST, in particular regarding specificity, PPV, and overall accuracy.

Contained sinus of Valsalva dissection into the left ventricular myocardium is an extremely rare condition [(1,2)][1]. A 19-year-old phenotypically normal man underwent mitral valve replacement for spontaneous chordal rupture. Discharge echocardiogram showed no evidence of abnormality in the

The left main coronary artery (LMCA) is responsible for supplying the majority of the left ventricular myocardium. Visual estimation of stenosis severity on angiography has major limitations and methods to assess functional significance, such as fractional flow reserve (FFR), have been shown to yield better outcomes; however, to date, major trials examining the use of such physiological indices have excluded LMCA disease. Furthermore, LMCA disease commonly co-exists with downstream disease, which complicates the interpretation of coronary physiological data. This review summarises existing evidence for physio-‌logy-guided management of LMCA disease. It will also explore the difficulties posed when functionally assessing LMCA lesions and outline potential solutions. Finally, we aim to provide insight into how novel physiological tools may improve the management of LMCA disease in the future.

Liver radiotracer activity interfering with the inferior myocardial wall in a patient undergoing myocardial perfusion imaging (MPI) with 99mTc-Sestamibi is a known pitfall. We report a patient with pituitary macroadenoma who was subjected to stress-MPI study for pre-anesthetic clearance. The post-stress raw image showed the liver radiotracer activity in close approximation to the anteroseptal wall of the left ventricular myocardium, secondary to right hemi-diaphragmatic eventration.

Echinococcal lesions rarely involve the heart; nonetheless, echinococcal cysts of the left ventricular myocardium often demand surgical treatment due to the risk of rupture and anaphylaxis. Herein, an echinococcal cyst of the anteroapical left ventricular wall was managed through small left anterior thoracotomy; repair was achieved under cardioplegic arrest (endoaortic balloon occlusion) with an uneventful course. We discuss the usefulness of such a less invasive approach for the depicted lesion (minimized manipulation of the heart and reduced surgical aggressiveness) and for other lesions involving the apical/lateral LV region.

Background: The high-temperature requirement serine peptidase 2 (HtrA2) is a pro-apoptotic mitochondrial serine protease involved in caspase-dependent as well as caspase-independent programmed cell death. When HtrA2 protein is tightly associated with mitochondria (MITO), its protease activity is masked. In contrast, once the protein is released from MITO into the cytosol (CS), its protease activity is exposed. Once active HtrA2 activates caspase-3, a pro-apoptotic enzyme, by degrading the caspase-3 inhibitor XIAP (x-linked inhibitor of apoptosis protein. Recent studies have shown that translocation of HtrA2 protein from the MITO to the CS occurs in mice hearts during experimental myocardial ischemic and reperfusion. Hypothesis: In this study we examined if translocation of HtrA2 from MITO to CS occurs in LV myocardium of dogs with chronic stable heart failure (HF). Methods: LV tissue from 7 dogs with chronic HF produced by multiple sequential intracoronary micro-embolizations (LV ejection fraction Results: GAPDH and porin protein levels were unchanged between NL and HF dogs. Compared to NL, HtrA2 protein levels in dogs with HF were unchanged in HG (0.76 ± 0.04 vs. 0.73 ± 0.08), significantly reduced in MITO (0.17 ± 0.02 vs. 0.40 ± 0.05, p Conclusions: Compared to NL dogs, HtrA2 protein levels are significantly reduced in MITO but increased in cytosol fractions from LV myocardium of dogs with chronic stable HF; a maladaptations that promotes cardiomyocyte apoptosis and progressive LV dysfunction. Inhibiting the translocation of HtrA2 from MITO to CS may have therapeutic potential for the preventing progressive dysfunction of the failing heart.

Background: There is a growing interest in the observed significant incidence of transthyretin cardiac amyloidosis in elderly patients with aortic stenosis. Approximately, 16% of patients with severe aortic stenosis undergoing aortic valve replacement have transthyretin cardiac amyloidosis. Outcomes after aortic valve replacement appear to be worst in patients with concomitant transthyretin cardiac amyloidosis. Method: Publications in PubMed, Cochrane Library, and Embase databases were systematically searched from January 2012 to September 2018 using the keywords transthyretin, amyloidosis, and aortic stenosis. All studies published in English that reported the prevalence, association and outcomes of transthyretin cardiac amyloidosis in patients with aortic stenosis undergoing were included. Results/Conclusion: The relationship between aortic stenosis and transthyretin cardiac amyloidosis is not well understood. A few studies have proven successful surgical management when both conditions coexist. This systematic review suggests that transthyretin cardiac amyloidosis is common in elderly patients with aortic stenosis and tend to have high mortality rates after AVR. The significant incidence of the two diseases occurring simultaneously warrants further investigation to improve management strategies in the future.

BACKGROUND The management of asymptomatic patients with aortic regurgitation (AR) and preserved left ventricular (LV) ejection fraction (LVEF) remains challenging. The purpose of the study was to assess the early changes of LV mechanics by 2D speckle-tracking echocardiography (2D-STE) in order to predict a decrease in LVEF. METHODS Sixty-seven patients (age, 47 ± 15 years) with asymptomatic moderate (n = 27) and severe AR (n = 40) with preserved LVEF were prospectively followed for about 5 years. Sixty healthy age-matched controls were included in the study. Standard echocardiography and 2D-STE were performed at the baseline and follow-up. The primary endpoint was a deterioration of the LVEF (≤50%). RESULTS At baseline, global LV longitudinal peak systolic strain (GLS) and strain rate (GLSRs) were decreased in patients with severe AR compared to controls (-18.9 ± 2.4 vs 20.0 ± 2.1%; -1.05 ± 0.19 vs -1.18 ± 0.15 1/s, P

Background Assessment of myocardial deformation from time-resolved cardiac computed tomography (4D CT) would augment the already available functional information from such an examination without incurring any additional costs. A deformable image registration (DIR) based approach is proposed to allow fast and automatic myocardial tracking in clinical 4D CT images. Methods Left ventricular myocardial tissue displacement through a cardiac cycle was tracked using a B-spline transformation based DIR. Gradient of such displacements allowed Lagrangian strain estimation with respect to end-diastole in clinical 4D CT data from ten subjects with suspected coronary artery disease. Dice similarity coefficient (DSC), point-to-curve error (PTC), and tracking error were used to assess the tracking accuracy. Wilcoxon signed rank test provided significance of tracking errors. Topology preservation was verified using Jacobian of the deformation. Reliability of estimated strains and torsion (normalized twist angle) was tested in subjects with normal function by comparing them with normal strain in the literature. Results Comparison with manual tracking showed high accuracy (DSC: 0.99± 0.05; PTC: 0.56mm± 0.47 mm) and resulted in determinant(Jacobian) > 0 for all subjects, indicating preservation of topology. Average radial (0.13 mm), angular (0.64) and longitudinal (0.10 mm) tracking errors for the entire cohort were not significant (p > 0.9). For patients with normal function, average strain [circumferential, radial, longitudinal] and peak torsion estimates were: [-23.5%, 31.1%, −17.2%] and 7.22°, respectively. These estimates were in conformity with the reported normal ranges in the existing literature. Conclusions Accurate wall deformation tracking and subsequent strain estimation are feasible with the proposed method using only routine time-resolved 3D cardiac CT.

We studied clinical and ultrasonographic parameters in pregnant women - 183 with and 152 without gestational arterial hypertension (GAP). Characteristics of women with GAP were as follows: age 16-45 years, mean age 27.9+/-4.7 years, disease duration 8.8+/-4.0 weeks, mean systolic and diastolic blood pressure at initial examination 150.2+/-4.8 and 93.1+/-6 mm Hg, respectively. Results of this study allowed us to make the following conclusions. Social, historical, constitutional parameters can contribute to the development of hypertension during pregnancy. GAP is associated with development of hypertrophy of left ventricular myocardium and its subsequent remodeling, hypertrophy and dilatation of the right ventricle, i.e. formation of morphological substrate for heart failure. Dynamics of echocardiographic structural-geometrical parameters of pregnant women with GAP is related to type and degree of hypertension.

Focal subendocardial/transmural low attenuation in the left ventricular myocardium (LVM) in cardiac CT represent fatty metaplasia after myocardial infarction (MI). However, the frequency of intramyocardial fat (IMF) in patients with no history of coronary artery disease (CAD) is unknown. We

Myocardial clefts are defined as narrow, deep blood-filled invaginations within the left ventricular myocardium. They occur in hypertrophic cardiomyopathy patients with different frequency and represent a distinctive morphological expression of hypertrophic cardiomyopathy. Although two-dimensional transthoracic echocardiography is able to detect myocardial clefts in some cases, cardiovascular magnetic resonance imaging with its high spatial resolution can detect myocardial clefts not visualized with echocardiography. In this report, we represent multimodality imaging of a septal myocardial cleft in a hypertrophic cardiomyopathy patient.

Background: Reactive aldehydes such as 4-hydroxy-2-nonenal (4-HNE) are generated in the failing heart and contribute to cardiomyocyte injury and death and progressive left ventricular (LV) dysfunction. Aldehyde dehydrogenase-2 (ALDH2) plays a pivotal role in detoxifying mitochondrial (MITO) reactive aldehydes. We previously showed that long-term therapy with Elamipretide (ELA, Bendavia TM ), a novel MITO targeting peptide, improves LV systolic function and normalizes MITO function and rate of ATP synthesis in dogs with heart failure (HF). In this study, we examined the effects of long-term treatment with ELA on protein levels of 4-HNE adducts and ALDH2 in LV myocardium of dogs with coronary microembolization-induced HF (LV ejection fraction ~30%). Methods: LV tissue from 14 HF dogs randomized to 3 months monotherapy with subcutaneous injections of ELA (0.5 mg/kg once daily, n=7) or saline (control, CTR, n=7) and tissue from 6 normal (NL) dogs was used in the study. Using LV tissue extracts, 4-HNE protein adducts levels were quantified using a commercially available Elisa kit and expressed as ng/mg. In isolated MITO fractions prepared from LV tissue, protein levels of ALDH2 and porin, the latter used as an internal loading control, were determined by Western blotting coupled with Chemiluminescence. Band intensity was expressed in densitometric units (DU). Results: No changes in protein level of porin was observed among the 3 study groups (NL: 0.26±0.02; CTR: 0.24±0.01; BEN: 0.26±0.01 DU). 4-HNE protein adducts levels were increased in CTR dogs compared to NL dogs and treatment with ELA partially restored 4-HNE to near normal levels (NL: 185±21; CTR: 399±35*; ELA: 252 ± 18† ng/mg, *=p Conclusions: Long-term therapy with ELA normalizes ALDH2 and 4-HNE levels in LV myocardium of dogs with HF. Improved protein levels of ALDH2 in HF after therapy with ELA can account, in part, for the observed improvement of global LV function elicited by long-term therapy with ELA.

Noncompaction of the left ventricular myocardium (LVNC) is a new clinical entity firstly described by Engberding and Bender in 1984. LVNC is characterized by the presence of numerous prominent trabeculations and deep intertrabecular recesses within the left ventricle. Recently, it has been demonstrated by two-dimensional (2D) speckle-tracking echocardiography (STE), that left ventricular (LV) basal and LV apical rotations are in the same direction resulting in the near absence of LV twist in LVNC patients, which was called as "LV solid/rigid body rotation." Three-dimensional (3D)-STE has just been introduced, and found to be an accurate method for the evaluation of LV rotation mechanics. The aim of this report was to confirm LV "rigid body rotation" in an LVNC patient by 3D-STE.

CT myocardial perfusion imaging is an emerging CT application using density measurements of contrast-enhanced left ventricular (LV) myocardium.Using a 320-MDCT we have consistently observed lower Hounsfield unit (HU) values in the lateral LV myocardium, potentially mimicking perfusion defects. This study aimed to evaluate contrast-enhancement patterns of the LV myocardium in normal studies.Twenty-one clinical cases with normal coronary MDCT-based angiography findings, as determined by 2 qualified readers, were selected for retrospective evaluation. Using 8 identically sized and positioned ROIs, the HU measurements were recorded from short axis axial reconstructions through the LV myocardium in middle, apical, and basal locations. Scans were acquired on a 320-slice MDCT unit.The middle short axis location demonstrated HU densities of 79.4 (range 42.3-162.7) in the lateral myocardial wall (regions 2, 3, and 4) compared with 103.9 (range 11.4-159.6) in the inferior, septal, and anterior walls (regions 1, 5, 6, 7, and 8; P0.001). HU densities for the basal slice were 82.3 (range 51.5-168.4) in the lateral wall compared with 94.9 (range 35.3-144) in the inferior, septal, and anterior walls (P0.001). In the apical location, HU densities were 79.9 (range 42.3-139.3) in the lateral wall compared with 100.9 (range 69.0-170.5) in the inferior, septal, and anterior walls (P0.001).Normal LV myocardial enhancement using a 320-slice MDCT demonstrates significantly lower densities in the lateral wall when compared with the anterior, septal, and inferior walls in patients with normal coronary vascular anatomy. Assessment of CT myocardial perfusion studies should therefore be undertaken with caution, to prevent misrepresenting these lower-density values in the LV lateral wall.

Background Owing to inconsistent diagnostic criteria and small heterogeneous cohorts, little is known about the long-term outcomes of adult left ventricular noncompaction (LVNC), a rare cardiomyopathy with potentially serious outcomes. This systematic overview aimed to better delineate the natural history of adult LVNC. Method and Results A comprehensive computerized search using “noncompaction” and its synonyms initially identified 206 articles, with reference lists subsequently hand scanned. These searches yielded 5 studies that were eligible for this systematic overview, identifying adult cohorts with isolated LVNC diagnosed by similar echocardiographic criteria. This combined cohort (n = 241) was followed for a mean duration of 39 months. The annualized event rate was 4% for cardiovascular deaths, 6.2% for cardiovascular death and its surrogates (heart transplantation and appropriate implantable cardioverter-defibrillator shocks), and 8.6% for all cardiovascular events (death, stroke, implantable cardioverter-defibrillator shocks, and heart transplantation.) Familial occurrence of LVNC in first-degree relatives was identified by echocardiography in 30% of index cases who were screened. Conclusion LVNC is an increasingly recognized cardiomyopathy diagnosed by echocardiography and is associated with familial tendencies, arrhythmias, thromboembolism, advanced heart failure, and death.

We report a case of streaky fat deposition and late hyperenhancement in the middle layer of the left ventricular myocardium detected on computed tomography coronary angiography and cardiac magnetic resonance imaging in a patient with dilated cardiomyopathy. CT revealed multiple curvilinear streaks of hypoattenuating foci involving the middle layer of the LV myocardium, with a mean attenuation value of -70 HU, comparable to that of fat. Late mid-wall hyperenhancement foci were noted in the fatty deposition sites of the left ventricle wall on delayed contrast-enhanced cardiac MRI. However, an area of late mid-wall hyperenhancement was smaller than that of fat deposition.

Significant proximal left anterior descending artery (LAD) disease may jeopardize up to 50% of the left ventricular myocardium [(1)][1] and predicts worse outcomes [(2)][2], with a significantly worse 5-year patient survival rate (90% vs. 98%) than downstream LAD lesions [(3)][3]. In the 1990s

Sirtuins are a highly conserved family of histone/protein deacetylases. In mammalian cells, seven sirtuins (SIRT1-7) modulate distinct metabolic and stress-response pathways, with SIRT3 having been most extensively investigated in the cardiovascular system and is mainly located in the mitochondria.

Cardiolipin (CL), an inner mitochondrial (MITO) membrane phospholipid is synthesized by CL synthase-1 (CLS1) and is critical for normal MITO function. Levels of CL are reduced in MITO of LV myocardium of dogs with heart failure (HF) and are normalized after chronic therapy with elamipretide (ELAM)

AIM To study tissue velocity imaging (TVI) and strain rate imaging (SRI) indices in akinetic nonviable and normal left ventricular (LV) inferobasal segment and effect of dobutamine infusion on these indices in nonviable segments. METHODS The study population consisted of two groups: 25 patients (mean age 60.75 +/- 8.69 years) with left ventricular akinetic inferobasal nonviable segment determined by dobutamine stress echocardiography (DSE) and 14 normal coronaries (mean age 56.67 +/- 11.90 years) with normal echocardiography as control group. The following TVI and SRI parameters were measured in patient and control group: ejection phase velocity (Sm [cm/sec]), peak systolic strain (ST [%]), and strain rate (SR [per second])). RESULTS Ejection fraction was significantly lower in patient group (29.40%+/- 5.46% vs. 55.00%+/- 3.39%; P < 0.001). Several differences were observed in patients with nonviable inferobasal segments compared to control group: Sm was reduced (3.58 +/- 1.08 cm/sec vs. 5.56 +/- 1.28 cm/sec; P < 0.001); SR and ST were significantly decreased (-0.39 +/- 0.20/second vs. -1.44 +/- 0.64/second, and -3.86%+/- 4.12% vs. -17.64%+/- 7.44%, respectively; P < 0.001 in both). The range of SR for nonviable segments (-0.04 to -0.77/second) did not overlap with that of the normal segments (-0.80 to -3.0/second). This range for Sm and ST overlapped with those of the normal segments. CONCLUSION All TVI and SRI parameters are reduced in akinetic nonviable inferobasal compared with normal segments. According to findings of this study, resting strain rate has a potential to discriminate nonviable inferobasal from normal segments.

Isolated noncompaction of the ventricular myocardium (INVM) is an uncommon cardiomyopathy characterized by the persistence of fetal myocardium with prominent trabecular meshwork and deep intertrabecular recesses, often associated with systolic dysfunction and ventricular dilatation. A 23-year-old man from Burkina Faso was referred to our operative unit with a diagnosis of INVM, made with echocardiogram and magnetic resonance imaging and nonsustained ventricular tachycardia. The literature reports the incidence of malignant ventricular arrhythmias in as many as 47% of the patients and sudden cardiac death in almost 50% of them and this supported our decision to perform implantable cardioverter-defibrillators implantation.

This experimental study investigated the impact of hyperglycemic control on left ventricular (LV) function using a model of diabetes mellitus (DM) (induced by streptozocin 60 mg/kg). Sixteen adult-Sprague Dawley rats were divided into group 1 (poor hyperglycemic control, n = 8) and group 2 (good hyperglycemic control, n = 8). Diabetic rats and 8 healthy rats serving as controls (group 3) were sacrificed on day 28 after DM induction. The results demonstrated that HbA1C on day 28 was higher in group 1 than in groups 2 and 3 (P < 0.0001). The mRNA expressions of MMP-9 and endothelin-1 were elevated in group 1 compared with that in groups 2 and 3 (P < 0.05), whereas PGC-1α and eNOS were lower in group 1 than in groups 2 and 3 (P < 0.05). The number of apoptotic nuclei was higher in group 1 than in groups 2 and 3 (P < 0.01). The integrated area (μm2) of connexin43 (Cx43), Cx43 protein expression, and LV function were lower in group 1 than in groups 2 and 3 (P < 0.05). Moreover, PKC-e expression in the mitochondrial compartment was decreased in group 1 compared to that in groups 2 and 3 (P < 0.005).

We report a case of a 55-year-old woman who has a non-compaction of the left ventricular myocardium diagnosed after a cardiac arrest due to a polymorphic ventricular tachycardia. The patient was implanted with a cardioverter-defibrillator. A review of literature of this recently described cardiopathy is done.

Aim: We aimed to present a case with ventricular myocardial noncom- paction involving both ventricles. Methods and results: Noncompaction of ventricle is a rare and unclassified congen- ital cardiac malformation is due to an arrest in intrauterine endomyocardial mor- phogenesis. We presented a ventricular myocardial noncompaction case involving both left and right ventricles. The physical examination of this case is consistent with mitral regurgitation and the echocardiographic findings are consistent with noncompaction of ventricular myocardium involving both ventricles with left ven- tricular systolic failure. Conclusion: Transthoracic echocardiography is a useful clinical tool for diagnosing noncompaction of both the right and left ventricular myocardium. The LVNC defini- tion can also be utilized for RVNC, which this diagnosis has never been reported in a Turkish patient. a 2005 Published by Elsevier Ltd on behalf of The European Society of Cardiology.

Background The most common cardiac tumors in young children are rhabdomyoma and fibroma, and prognosis depends on the tumor's characteristics. In the present study electron-beam computed tomography (EBT) was used to evaluate tumor characteristics and myocardial perfusion in 6 children with cardiac tumors. Methods and Results Five children had rhabdomyomas and 1 had a fibroma. In the precontrast study, the computed tomography numbers of rhabdomyomas were higher and those of the fibroma were slightly lower than those of the normal myocardium. In the early postcontrast study, the size, location, shape and number of the tumor were clearly detected, and in the late postcontrast study, the fibrous characteristics of the tumor were seen. The fibroma contained calcification and 2 rhabdomyomas contained a fat density spot. In the cine-mode study, both the tumor and ventricular wall motion could be simultaneously evaluated. There was a filling defect of the left ventricular myocardium on the early postcontrast scan of 1 child with a rhabdomyoma and dyskinetic wall motion at the same region in the cine-mode study. Conclusion EBT was useful for evaluating tumor characteristics in children. (Circ J 2005; 69: 1352 - 1356)

Serum testing for the hormone B-type natriuretic peptide (BNP) may have clinical utility in congestive heart failure (CHF). This hormone is secreted predominantly by the left ventricular myocardium in patients with CHF. Measurement of serum BNP may improve diagnosis of CHF and may also help guide therapy in patients with CHF. The literature regarding the clinical utility of BNP measurement in CHF is reviewed.

Few data have been published on the reproducibility of baseline subtracted peak intensity obtained from intravenous intermittent triggered myocardial contrast echocardiography. We investigated the reproducibility of the peak intensity measured from intravenous intermittent triggered myocardial contrast echocardiography in 10 young healthy males. The contrast echocardiography was obtained using the second harmonic mode with an intravenous bolus injection of Levovist (first study). The same myocardial contrast echocardiography was repeated after the first study (second study). The myocardial opacification and peak intensity in the 12 segments of the apical 4 and 2 chamber views were assessed visually and quantitatively. The differences in the peak intensity between the initial and repeated measurements in the first study (intraobserver reproducibility) and between the initial measurements in the first and second studies (interinjection reproducibility) were assessed using the Bland and Altman method. The degree of opacification was good or intermediate in 207/228 (91%) of the segments. The agreement of myocardial opacification between the first and second studies was 87/114 (76%). However, significantly higher peak intensity was obtained in apical septal (8200 +/- 6300 au2) and mid septal (8500 +/- 6000 au2) segments in the 4 chamber view and in the mid inferior (12400 +/- 9300 au2) and apical inferior (10700 +/- 6300 au2) segments in the 2 chamber view compared with other segments. The mean differences of the peak intensities according to the Bland and Altman analysis was -1600 +/- 5000 au2 in the intraobserver reproducibility study, and -1100 +/- 5300 au2 in the interinjection reproducibility study. Thus, the measurement error was determined to range from 8400 au2 to 9500 au2 in both studies. We conclude that the peak intensity obtained from intravenous intermittent triggered myocardial contrast echocardiography using Levovist varies significantly among segments in the left ventricular myocardium. Large intraobserver and interinjection variability exists in the measurement of peak intensity, suggesting that the reproducibility of this technique is limited for quantitative assessment of myocardial perfusion.