Myocardial Mechano-energetic Efficiency Research Articles

Myocardial mechano-energetic efficiency is not impaired in patients with metabolically healthy overweight and obesity.

Reduced myocardial mechano-energetic efficiency (MEE) was associated with BMI. Subgroups of individuals with increased BMI but favorable cardiovascular risk profile were identified as individuals with "metabolically healthy overweight" (MHOW) and "metabolically healthy obesity" (MHO), respectively. We aim to investigate whether those with MHOW/MHO, defined as those having none of the components of metabolic syndrome, exhibit impaired MEE compared with their unhealthy counterparts. Myocardial MEE per gram of left ventricular mass (MEEi) was assessed by echocardiography in 2190 nondiabetic individuals participating in the CATAnzaro MEtabolic RIsk factors (CATAMERI) study who were divided, according to BMI and metabolic status, into groups of individuals with metabolically healthy normal weight (MHNW), metabolically unhealthy normal weight (MUNW), MHOW, metabolically unhealthy overweight (MUOW), MHO, and metabolically unhealthy obesity (MUO). After adjusting for age and sex, no differences in myocardial MEEi were observed among individuals with MHNW, MHOW, and MHO (p = 0.56). Myocardial MEEi was comparable among individuals with MUNW, MUOW, and MUO (p = 0.21). Individuals with MHNW, MHOW, and MHO displayed significantly higher myocardial MEEi compared with their unhealthy counterparts. Increased BMI is not an obligate determinant for reduced myocardial MEEi. Other known components of metabolic syndrome rather than increased BMI contributed to reduced myocardial MEEi.

Whole blood viscosity is associated with reduced myocardial mechano-energetic efficiency in nondiabetic individuals.

This cross-sectional study aimed to investigate the association between myocardial mechano-energetic efficiency (MEE) and whole blood viscosity (WBV) in nondiabetic adults participating in the CATAnzaro MEtabolic RIsk factors (CATAMERI) study. 1143 participants underwent an oral glucose tolerance test and an echocardiogram for myocardial MEE per gram of left ventricular mass (MEEi) measurement. WBV was measured as: [0.12 × h] + [0.17 × (p-2.07)], where h is haematocrit and p is plasma protein levels. Study population includes 595 males and 548 females with a mean age of 46 ± 12 years and a mean BMI of 30.0 ± 6.2 kg/m2 . Individuals with normal glucose tolerance were 63%, while those with impaired fasting glucose, impaired glucose tolerance and or the combination of both were 14.3%, 13% and 9.7%, respectively. A univariate analysis showed that MEEi was significantly associated with sex, age, smoking, BMI, waist circumference, total cholesterol, HDL, triglycerides, fasting glucose, fasting insulin, HOMA-IR index, glucose tolerance, C-reactive protein, haematocrit, haemoglobin, plasma protein and WBV. In a multivariable regression model including variables that were significantly associated with MEEi in univariate analysis, MEEi was associated with HOMA-IR (β = -0.144, p < .001), age (β = -0.140, p < .001), WBV (β = -0.129, p < .001) and glucose tolerance (β = -0.064, p = .04). The independent association between WBV and MEEi remained statistically significant (β = -0.122, p < .001) when antihypertensive therapy and lipid-lowering therapy were included in the model. WBV is associated with decreased myocardial MEE independently of other cardiovascular risk factors.

Mechano-energetic efficiency in patients with hypertrophic cardiomyopathy with and without sarcomeric mutations.

Hypertrophic cardiomyopathy (HCM) is mainly caused by sarcomeric mutations which may affect myocardial mechano-energetic efficiency (MEE). We investigated the effects of sarcomeric mutations on MEE. A non-invasive pressure/volume (P/V) analysis was performed. We included 49 genetically screened HCM patients. MEEi was calculated as the ratio between stroke volume and heart rate normalized by LV mass. Fifty-seven percent (57%) HCM patients carried a sarcomeric mutation. Patients with and without sarcomeric mutations had similar LV ejection fraction, heart rate, LV mass, and LV outflow gradient. Younger age at diagnosis, family history of HCM, and lower MEEi were associated with presence of sarcomeric mutation (p = 0.017; p = 0.001 and p = 0.0001, respectively). Lower MEEi in HCM with sarcomeric mutation is not related to significant differences on filling pressure as shown on P/V analysis. Sarcomeric mutations determine a reduction of the LV pump performance as estimated by MEEi in HCM. Lower MEEi may predict a positive genetic analysis.

Endothelial dysfunction is associated with reduced myocardial mechano-energetic efficiency in drug-naïve hypertensive individuals.

Impaired myocardial mechano-energetics efficiency (MEE) was shown to predict incident heart failure, but pathophysiological mechanisms linking impaired MEE with heart failure have not been elucidated. Endothelial dysfunction is a plausible candidate because it has been associated with heart failure. This study aims to investigate the association between MEE and endothelium-dependent vasodilation, among drug-naïve hypertensive individuals. 198 Drug-naïve hypertensive individuals participating in the CATAnzaro MEtabolic RIsk factors (CATAMERI) study were included. All participants underwent to an oral glucose tolerance test and to an echocardiogram for myocardial LVM-normalized mechano-energetic efficiency (MEEi) measurement. Endothelial-dependent and endothelial-independent vasodilatation were measured by strain-gauge plethysmography during intra-arterial infusion of acetylcholine and sodium nitroprusside, respectively. A multivariate linear regression analysis was conducted to investigate the independent association between maximal endothelial-dependent vasodilation and MEEi. Maximal ACh-stimulated forearm blood flow (FBF) was associated to decreased myocardial MEEi (β = 0.205, p = 0.002) independently of well-established cardiovascular risk factors including age, sex, BMI, waist circumference, smoking status, total and HDL cholesterol, triglycerides, hsCRP, glucose tolerance status, and HOMA-IR index of insulin resistance. Conversely, no association was observed between SNP-stimulated vasodilation and MEEi. Endothelium-mediated vasodilation may contribute to reduce myocardial MEEi independently of several potential confounders. Because diminished myocardial MEE has been previously associated with incident heart failure, a non-invasive assessment of myocardial MEEi may improve the identification of individuals at higher cardiovascular risk who may benefit from the initiation of pharmacological treatments ameliorating the endothelial dysfunction.

INDEPENDENT ASSOCIATION BETWEEN URIC ACID LEVELS AND MYOCARDIAL MECHANO-ENERGETIC EFFICIENCY AS ASSESSED BY ECHOCARDIOGRAPHY

Objective: In the last decades several studies have investigated the relationship between serum uric acid (SUA) levels and cardiovascular disease and heart failure. Low myocardial mechano-energetic efficiency (MEE), estimated as stroke volume/heart rate ratio per g of left ventricular (LV) mass (LVM) is an independent predictor of cardiovascular (CV) events and heart failure. Design and method: Aim of the study was to evaluate the relationship between SUA and myocardial mechano-energetic efficiency index (MEEi) in 694 consecutive uncomplicated patients attending the outpatient at an ESH Excellence Centre in Italy. Methods BP values were measured by the physician with an automated oscillometric device, after 5 minutes of rest. All patients underwent transthoracic echocardiography, and standard indices of systolic function were calculated. In all patients myocardial mechanoenergetic efficiency (MEE) was calculated as stroke volume/heart rate and indexed to LV mass (MEEi = MEE/LVM) (de Simone et al, 2016). Results: Results Mean age was 57±13 yrs, 52% female, 21 % obese, 10 % diabetics, 69 % with a previous diagnosis of hypertension (77 % treated). MEEi was lower in males (0.42±0.14 vs 0.49±0.16, p&lt;0.001), and in patients with diabetes (0.38±0.11 vs 0.47±0.16, p&lt;0.001). At multivariate analysis the variables independently correlated with MEEI were male sex, systolic blood pressure, presence of obesity, plasma glucose levels, and serum uric acid, but not age and eGFR (CKD EPI). At receiver operating curves (ROC) analysis the optimal cutoff of uric acid for the prediction on reduced MEEI was 5.4 mg/dl (AUC 0.611. 95 CI 0.574-0.648). Conclusions: Conclusions In a large sample of uncomplicated patients attending the outpatient clinic at an ESH Excellence Centre in Italy uric acid is an independent predictor of myocardial mechanoenergetic efficiency. In this population the optimal cutoff of uric acid for reduced MEEI is 5.4 mg/dl. These findings may contribute to the explanation of the greater risk of heart failure in patients with increased uric acid levels.

MYOCARDIAL MECHANO-ENERGETIC EFFICIENCY AND CLINIC AND 24 HOURS BLOOD PRESSURE VALUES IN PATIENTS ATTENDING THE OUTPATIENT CLINIC AT AN ESH EXCELLENCE CENTRE IN ITALY

Objective: It has been demonstrated that low myocardial mechano-energetic efficiency index (MEEi),estimated as stroke volume/heart rate ratio per g of left ventricular(LV) mass(LVM) is an independent predictor of cardiovascular(CV) events. Out of office blood pressure (BP) is better correlated to hypertension mediated organ damage(HMOD) and to CV events as compared to BP measured in the office. Design and method: Aim of the study was to evaluate the relationship between myocardial mechano-energetic efficiency index and both clinic and 24 hours BP values in 839 consecutive uncomplicated patients attending the outpatient at an ESH Excellence Centre in Italy. Methods BP values were measured by the physician with an automated oscillometric device, after 5 minutes of rest. ABPM was performed in all subjects with a Spacelabs BP monitor. All patients underwent transthoracic echocardiography, and standard indices of systolic function were calculated. Furthermore in all patients myocardial mechanoenergetic efficiency (MEE) was calculated as stroke volume/heart rate and indexed to LV mass (MEEi=MEE/LVM) (de Simone et al, 2016). Results: Mean age was 53 ± 14 yrs, 53% female, BMI 26 ± 5, 34 % were overweight, 18% obese, 8% % diabetics, 64 % with a previous diagnosis of hypertension(71 % treated). MEEi was lower in males (0.41 ± 0.14 vs 0.52 ± 0.15), and in patients with diabetes(0.40 ± 0.11 vs 0.48 ± 0.16). MEEi was inversely -correlated with age(r = -0.146, p &lt; 0.0001) and BMI(r = -0.353, p &lt; 0.0001). MEEI was similarly correlated to 24 hours SBP and clinic SBP(respectively r = -0.267, p &lt; 0.0001 and r = -0.196, p &lt; 0.001, Steiger's Z test for the comparison p ns) and to 24 hours DBP and clinic DBP(r = -0.249, p &lt; 0.0001 and r = -0.248, p &lt; 0.001, Steiger's Z test for the comparison p ns). However, at receiver operating curves(ROC) the area under the curve(AUC) for 24 hours SBP(0.627, 95 % CI 0.593 - 0.659) was superior in predicting low MEEI (defined as &lt; 0.35) as compared to the AUC of clinic SBP(0.582, 95 % CI 0.548 - 0.615)(p for the comparison &lt; 0.05). Conclusions: In a large sample of uncomplicated patients attending the outpatient clinic at an ESH Excellence Centre in Italy 24 hours BP is a better predictor of reduced myocardial myocardial mechanoenergetic efficiency than clinic BP.

Metabolic Syndrome and C-reactive Protein are Associated With a Reduced Myocardial Mechano-energetic Efficiency.

Metabolic syndrome and elevated high-sensitivity C-reactive protein (hsCRP) levels are associated with risk of cardiovascular diseases. A reduced myocardial mechano-energetic efficiency (MEE) has been found to be an independent predictor of cardiovascular disease. To evaluate the association between metabolic syndrome and hsCRP levels with impaired MEE. Myocardial MEE was assessed by a validated echocardiography-derived measure in 1975 nondiabetic and prediabetic individuals subdivided into 2 groups according to the presence of metabolic syndrome. Individuals with metabolic syndrome exhibited increased stroke work and myocardial oxygen consumption estimated by rate pressure product, and a reduced MEE per gram of left ventricular mass (MEEi) compared with subjects without metabolic syndrome, after adjusting for age and sex. Myocardial MEEi progressively decreased in parallel with the increase in the number of metabolic syndrome components. In a multivariable regression analysis, both metabolic syndrome and hsCRP contributed to reduced myocardial MEEi independently of sex, total cholesterol, high-density lipoprotein, triglycerides, fasting, and 2-hour postload glucose levels. When the study population was divided into 4 groups by the presence or absence of metabolic syndrome and by hsCRP levels above and below 3 mg/L, hsCRP levels ≥3 mg/L were associated with reduced myocardial MEEi both in subjects with metabolic syndrome and in those without the syndrome. Nondiabetic and prediabetic individuals with metabolic syndrome exhibit increased stroke work and myocardial oxygen consumption, and an impaired MEEi, an established predictor of adverse cardiovascular events, and elevated hsCRP levels in combination with metabolic syndrome aggravate the myocardial MEEi impairment.

C53 EFFECTS OF CARDIAC CONTRACTILITY MODULATION THERAPY ON LEFT VENTRICLE GLOBAL LONGITUDINAL STRAIN AND MYOCARDIAL MECHANO–ENERGETIC EFFICIENCY IN PATIENTS WITH HEART FAILURE WITH REDUCED EJECTION FRACTION

Abstract Background Impairment of myocardial mechano–energetic efficiency (MEE) is present in virtually all patients with heart failure with reduced ejection fraction (HFrEF). Cardiac contractility modulation (CCM) improves the quality of life and functional capacity, reduces hospitalizations, and induces biventricular reverse remodeling in patients with HFrEF. However, the effects of this innovative therapy on mechano–energetics efficiency and global longitudinal strain (GLS) are still unknown; therefore, the aim of this study is to evaluate whether CCM therapy can improve the MEE of patients with HFrEF. Methods We enrolled 25 patients with HFrEF who received an Optimizer Smart implant (the device that develops CCM therapy) between January 2018 and January 2021. Clinical and echocardiographic data were obtained from all patients 24 hours before and six months after CCM therapy. Results At six months, follow–up patients who underwent CCM therapy showed an increase of left ventricular ejection fraction (30.8+7.1 vs. 36.1+6.9%; p = 0.032) as well a rise of GLS 10.3+2.7 vs.–12.9+4.2; p = 0.018), of MME (32.2 + 10.1 vs. 38.6 + 7.6 mL/s; p = 0.013) and of MEE index (18.4 + 6.3 vs 24.3 + 6.7 mL/s/g; p = 0.022). Conclusions CCM therapy increased left ventricular performance, improving left ventricular ejection fraction, GLS, as well as MEE and MEEi.

Association between liver fibrosis and decreased myocardial mechano-energetic efficiency in individuals with different degree of glucose tolerance

AimDecreased myocardial mechano-energetic efficiency (MEEi) is associated with NAFLD and poorer prognosis in liver cirrhosis. We aim to investigate the association between liver fibrosis severity and MEEi in individuals participating in the CATAnzaro MEtabolic RIsk factors (CATAMERI) study. MethodsMyocardial MEEi, assessed by an echocardiography-derived measure, and fibrosis severity, estimated by the fibrosis-4 index (FIB-4), were evaluated in 2383 subjects with different degree of glucose tolerance. Participants were divided into four groups according to FIB-4 index values: lowest risk of fibrosis (<1.3); low risk of fibrosis (≥1.3 to < 1.67); moderate risk of fibrosis (≥1.67 to < 2.67); high risk of fibrosis (≥2.67). ResultsSubjects with higher risk of liver fibrosis displayed a graded decrease in myocardial MEEi compare to those with the lowest risk of liver fibrosis. In a multivariable regression analysis, FIB-4 index was independently associated with MEEi (β = -0.080, P < 0.001), along with total cholesterol (β = -0.067, P = 0.01), hsCRP (β = -0.081, P < 0.001), sex (β = -0.099, P < 0.001), glucose tolerance status (β = -0.109, <0.001) and HOMA-IR index (β = -0.143, P < 0.001). ConclusionCompromised myocardial MEEi is already reported in individuals with high risk of hepatic fibrosis suggesting that its assessment may help to identify among subjects with NAFLD those with worst prognosis.

Impaired insulin-stimulated myocardial glucose metabolic rate is associated with reduced estimated myocardial energetic efficiency in subjects with different degrees of glucose tolerance

BackgroundAlterations in myocardial mechano-energetic efficiency (MEEi), which represents the capability of the left ventricles to convert the chemical energy obtained by oxidative metabolism into mechanical work, have been associated with cardiovascular disease. Although whole-body insulin resistance has been related to impaired myocardial MEEi, it is unknown the relationship between cardiac insulin resistance and MEEi. Aim of this study was to evaluate the relationship between insulin-stimulated myocardial glucose metabolic rate (MrGlu) and myocardial MEEi in subjects having different degrees of glucose tolerance.MethodsWe evaluated insulin-stimulated myocardial MrGlu using cardiac dynamic positron emission tomography (PET) with 18F-Fluorodeoxyglucose (18F-FDG) combined with euglycemic-hyperinsulinemic clamp, and myocardial MEEi in 57 individuals without history of coronary heart disease having different degrees of glucose tolerance. The subjects were stratified into tertiles according to their myocardial MrGlu values.ResultsAfter adjusting for age, gender and BMI, subjects in I tertile showed a decrease in myocardial MEEi (0.31 ± 0.05 vs 0.42 ± 0.14 ml/s*g, P = 0.02), and an increase in myocardial oxygen consumption (MVO2) (10,153 ± 1375 vs 7816 ± 1229 mmHg*bpm, P < 0.0001) as compared with subjects in III tertile. Univariate correlations showed that insulin-stimulated myocardial MrGlu was positively correlated with MEEi and whole-body glucose disposal, and negatively correlated with waist circumference, fasting plasma glucose, HbA1c and MVO2. In a multivariate regression analysis running a model including several CV risk factors, the only variable that remained significantly associated with MEEi was myocardial MrGlu (β 0.346; P = 0.01).ConclusionsThese data suggest that an impairment in insulin-stimulated myocardial glucose metabolism is an independent contributor of depressed myocardial MEEi in subjects without history of CHD.

Association of low mechano-energetic efficiency and prognosis in liver cirrhosis.

In cirrhosis, cardiac systolic dysfunction as part of cirrhotic cardiomyopathyaffects prognosis. Myocardial mechano-energetic efficiency (MEE) is an estimate of left ventricular performance. In this study we investigated the relation of MEE to patient characteristics and its impact on survival in patients with cirrhosis. We included 283 patients with cirrhosis of different severity according to the Child-Pugh classifications (A/B/C: 106/87/90). All patients had a liver vein catheterization and a hemodynamic investigation performed including determination of cardiac output (CO), stroke volumeand heart rate (HR). These data were used to assess MEE, which was defined as (stroke volume/HR) × 1.666. Eighty-nine percent of patients had portal hypertension (hepatic venous pressure gradient >5 mmHg) and 80% indications of hyperdynamic circulatory state (increased CO and HR). There was no difference in MEE in Child-Pugh class C patients (2.03) versus Child-Pugh class A (1.98) and B (2.05) patients. In Child-Pugh class C patients, low MEE was associated with a poorer prognosis. In our study, MEE does not seem to be associated with severity of the liver disease, but in patients with advanced disease low MEE is associated with a poorer prognosis. The prognostic impact of MEE should be further investigated.

The Effects of Device-Based Cardiac Contractility Modulation Therapy on Left Ventricle Global Longitudinal Strain and Myocardial Mechano-Energetic Efficiency in Patients with Heart Failure with Reduced Ejection Fraction.

Background: Virtually all patients with heart failure with reduced ejection fraction have a reduction of myocardial mechano-energetic efficiency (MEE). Cardiac contractility modulation (CCM) is a novel therapy for the treatment of patients with HFrEF, in whom it improves the quality of life and functional capacity, reduces hospitalizations, and induces biventricular reverse remodeling. However, the effects of CCM on MEE and global longitudinal strain (GLS) are still unknown; therefore, this study aims to evaluate whether CCM therapy can improve the MEE of patients with HFrEF. Methods: We enrolled 25 patients with HFrEF who received an Optimizer Smart implant (the device that develops CCM therapy) between January 2018 and January 2021. Clinical and echocardiographic evaluations were performed in all patients 24 h before and six months after CCM therapy. Results: At six months, follow-up patients who underwent CCM therapy showed an increase of left ventricular ejection fraction (30.8 ± 7.1 vs. 36.1 ± 6.9%; p = 0.032) as well a rise of GLS 10.3 ± 2.7 vs. −12.9 ± 4.2; p = 0.018), of MEE (32.2 ± 10.1 vs. 38.6 ± 7.6 mL/s; p = 0.013) and of MEE index (18.4 ± 6.3 vs. 24.3 ± 6.7 mL/s/g; p = 0.022). Conclusions: CCM therapy increased left ventricular performance, improving left ventricular ejection fraction, GLS, as well as MEE and MEEi.

Mechano-energetic efficiency in patients with hypertrophic cardiomyopathy with and without sarcomeric mutations

Abstract Background Hypertrophic Cardiomyopathy (HCM) is mainly caused by sarcomeric mutations. In about 40% of cases the causal mutation is unknown. Myocardial mechano-energetic efficiency per unit of left ventricular (LV) mass (MEEi) is an echocardiographic parameter of LV pump performance. Sarcomeric mutations may affect energy efficiency. Purpose We investigated the effects of the presence of sarcomeric mutations on MEEi in patients with HCM. Methods We included 49 genetically screened HCM patients (50±10 years, 27% women) with LV ejection fraction &amp;gt;50%, LV maximal wall thickness &amp;gt;14 mm and no moderate to severe mitral regurgitation. MEEi was calculated as the ratio between stroke volume and heart rate, normalized by LV mass. Echo-LV mass was calculated as LV epicardial minus LV endocardial volumes in 4 and 2 chamber views multiplied by 1.05, a method validated with nuclear magnetic resonance. Results 27 HCM patients carried a sarcomeric mutation (HCM-Sarc; 55%). As shown in the table, patients with and without sarcomeric mutations (HCM-Sarc vs HCM-NoSarc) had similar LV ejection fraction, heart rate, LV mass and LV outflow tract gradient. HCM-Sarc showed early age at diagnosis, higher frequency of HCM family history and significantly reduced MEEi as compared with HCM-NoSarc. Presence of sarcomeric mutation could be predicted by younger age, lower MEEi and by family history of HCM (overall p&amp;lt;0.05). Conclusions In a population of HCM patients, the presence of a sarcomeric mutation is the only determinant of reduced the LV pump performance as estimated by MEEi. MEEi may be used as an imaging biomarker in sarcomeric mutation carriers. Funding Acknowledgement Type of funding sources: None.

Effects of 3 months of treatment with empagliflozin on left ventricle global longitudinal strain and myocardial mechano-energetic effiency.

Sodium glucose transporter-2 (SGLT-2) inhibitors are employed in the treatment of cardiovascular diseases such as heart failure and coronary artery disease. In the present study, we aimed to investigate how Empagliflozin in SGLT 2 inhibitors affects cardiac contraction and pump efficiency in patients who have Diabetes Mellitus (DM) without cardiovascular disease. The conventional echocardiographic records and biochemical values ​​of 62 patients who had DM without a history of cardiovascular disease were evaluated before using Empagliflozin. The myocardial mechano-energetic (MME) activity and index, and global longitudinal strain (GLS) were also calculated. After 3 months of Empagliflozin use, the tests were repeated and compared with previous data. A p<.05 was considered statistically significant. Left ventricular GLS and MME efficiency were found to be significantly higher after treatment (-17.71±2.12, -19.15±.71; p<.001 and 62.14±18.21, 72.24±26.57; p: .019). An increase was detected in left ventricular longitudinal strain and MME efficiency after using Empagliflozin for 3 months in patients with DM. This result suggests that Empagliflozin improves left ventricular pump efficiency and contraction.

Physiologic Range of Myocardial Mechano-Energetic Efficiency among Healthy Subjects: Impact of Gender and Age.

Background: Myocardial mechano-energetic efficiency (MEE) is the capability of the left ventricle (LV) to convert the chemical energy obtained from the cardiac oxidative metabolism into mechanical work. The aim of present study was to establish normal non-invasive MEE and MEEi reference values. Methods: In total, 1168 healthy subjects underwent physical examinations, clinical assessment, and standardized transthoracic echocardiographic (TTE) examination. MEE was obtained by TTE as the ratio between stroke volume (SV) and heart rate (HR): MEE = SV/HR [HR expressed in seconds (HR/60)]. Because MEE is highly related to left ventricular mass (LVM), MEE was then divided by LVM with the purpose of obtaining an estimate of energetic expenditure per unit of myocardial mass (i.e., indexed MEE, MEEi, mL/s/g). Results: The mean values of MEE and MEEi in the overall population were 61.09 ± 18.19 mL/s; 0.45 ± 0.14, respectively. In a multivariable analysis, gender, body surface area (BSA), diastolic blood pressure, left atrial volume indexed to BSA, E/e’ and tricuspid annular plane systolic excursion (TAPSE) were the independent variables associated with MEE, while age, gender, BSA and TAPSE were the independent variables associated with MEEi. Conclusions: The knowledge of age- and gender-based MEE and MEEi normal values may improve the global assessment of LV cardiac mechanics and serve as a reference to identify phenotypes at high risk of cardiovascular events.

Inappropriate left ventricular mass after HELLP syndrome inappropriate LVM after HELLP syndrome.

Excessive left ventricular mass (LVM) results in inefficient LV work with energy waste leading to a negative prognostic effect. We aimed at investigating the presence of inappropriate LVM and calculating the myocardial mechano-energetic efficiency index (MEEi) in former pre-eclamptic (PE) women (with or without HELLP syndrome) compared to women who experienced HELLP syndrome without PE. In this cross-sectional study, women with a history of normotensive HELLP (n=32), PE without HELLP (n=59), and PE with HELLP (n=101) underwent echocardiography as part of the clinical CV work-up after their complicated pregnancies from 6months to 4years postpartum. We excluded women with comorbidities, including chronic hypertension, hypercholesterolemia, and obesity. LVM excess was calculated as the ratio between observed LVM and predicted LVM (by sex, stroke work and height), while MEEi was considered as the ratio between stroke work and "double product" (to approximate energy consumption), indexed to LVM. LV hypertrophy was present in 8-14% and concentric remodeling in 31-42% of women, without intergroup difference. LVM was inappropriate in one-third of normotensive former HELLP and in about one-half of PE with or without HELLP, with no difference among groups. Accordingly, without nominal difference, MEEi showed a tendency towards lower values in former pre-eclamptic individuals. Women with a history of HELLP syndrome, independently from the presence/absence of PE, showed inappropriate LVM in the first 4years after delivery, which may partially explain the elevated CV risk in these women compared to the general female population.

Obstructive sleep apnea is associated with depressed myocardial mechanoenergetics.

To evaluate the association between the myocardial mechanoenergetic efficiency index (MEEi) and the Apnea-Hypopnea Index (AHI) in the initial phase of obstructive sleep apnea (OSA) diagnosis. In this cohort study, we included a total of 382 eligible participants without cardiovascular disease in a tertiary outpatient clinic between January 2013 and January 2015. We recorded demographic, clinical, polysomnographic and echocardiographic variables of the patients. In addition, myocardial mechanoenergetic efficiency (MEE) and MEEi were calculated by an echocardiography-derived validated measurement. The mean (±SD) age of the participants was 48.47 ± 12.13, and male/female ratio was 287/95. Comparing with non-OSA, MEEi was significantly lower in OSA patients at all stages (0.35 ± 0.08 vs. 0.42 ± 0.05; p< .001). MEEi was negatively correlated with hypertension (r= -0.518, p< .001), body mass index (r= -0.382, p< .001), AHI (r= -0.656, p< .001), total apne (r= -0.525, p< .001), hypopnea (r= -0.415, p< .001), systolic pulmonary pressure (r= -0.318, p< .001), relative wall thickness (RWT; r= -0.415, p< .001), and positive correlated with left ventricular ejection fraction (r= 0.586, p< .001). According to multiple linear regression analysis AHI (β= -0.625, p< .001), total apnea (β= -0.402, p= .001), hypopnea (β= -0.395, p= .001), LV ejection fraction (β= 0.478, p< .001) and RWT (β= -0.279, p< .001) have an independent relationship with MEEi. MEEi was lower in OSA patients. A reduced MEEi may reflect a disturbance in energy use of the myocardium. Consequently, our results may provide insight into the mechanisms leading to structural cardiac diseases in OSA patients.

Low myocardial mechano-energetic efficiency is an independent predictor of prognosis in advanced chronic liver disease.

We aimed at investigating if a low myocardial mechano-energetic efficiency (MEE) with energy waste could be a feature of cirrhotic cardiomyopathy and predictive of poor prognosis. We retrospectively interrogated a large data set of 115 cirrhotic patients followed up for 6 years and compared with 50 healthy controls. Echocardiographic and haemodynamic parameters were assessed at baseline according with current guidelines. MEE was estimated by echocardiographic stroke volume (z-derived)/(heart rate × 0.6). Cirrhotic patients presented low peripheral vascular resistance, a compensatory hyperdynamic syndrome with increased cardiac work, left atrial and left ventricular (LV) dimension and mass. Systolic parameters and MEE were similar between patients and controls. Patients with cirrhosis and refractory ascites showed significantly lower MEE compared with both patients with treatable ascites and patients without ascites (1.68 ± 0.47 vs. 1.98 ± 0.64 and 1.80 ± 0.37 ml/s; P < 0.05). Increased age and heart rate and reduced body weight, cardiac dimension and work significantly correlated with lower MEE, mostly when compared nonalcoholic with alcoholic cirrhosis (1.65 ± 0.42 vs. 1.95 ± 0.56 ml/s respectively; P = 0.002). Among the cardiovascular parameters left atrium enlargement and reduced MEE were independent predictors of death. In advanced chronic liver disease left ventricular performance is blunted due to an energetically inefficient cardiac mechanical work which correlates with a poor prognosis. Therefore, the simple basal assessment of MEE can identify patients with a worst prognosis which requires a close follow-up.

Depressed myocardial mechano-energetic efficiency in subjects with dysglycemia

AimsEvidence indicate that 1 h post-load glucose levels (1hPG) ≥ 155 mg/dl identify amongst subjects with normal glucose tolerance (NGT) a new category of prediabetes (NGT 1 h-high). A compromised myocardial mechano-energetic efficiency (MEE) is associated with type 2 diabetes and predicts adverse cardiovascular outcomes. Herein, we explored the association between prediabetes conditions such as NGT 1 h-high, impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) and a decreased MEE. MethodsMEE was assessed by an echocardiography-derived measure in 1467 non-diabetic individuals subdivided according to their glucose tolerance: NGT and 1-hPG < 155 mg/dl (NGT 1 h-low, n = 617), NGT 1 h-high (n = 210), isolated IFG (n = 237), and IGT (n = 403). ResultsSubjects with NGT 1 h-high, isolated IFG, and IGT displayed a higher myocardial oxygen consumption, and a decreased MEE in comparison to NGT 1 h-low group. MEE was inversely related to male sex, age, body mass index, total cholesterol, triglycerides, fasting and post-load glucose and insulin, C reactive protein, and positively correlated with insulin sensitivity estimated by the Matsuda index. In a stepwise multivariate linear regression model including several cardio-metabolic risk factors, 1hPG was the major predictor of MEE. ConclusionsSubjects with NGT 1 h-high, isolated IFG, and IGT have a raised myocardial oxygen consumption and a reduced MEE.

Sex-specific differences in left ventricular mass and myocardial energetic efficiency in non-diabetic, pre-diabetic and newly diagnosed type 2 diabetic subjects

BackgroundWomen with type 2 diabetes (T2DM) have a higher excess risk for cardiovascular disease (CVD) than their male counterparts. However, whether the risk for CVD is higher in prediabetic women than men is still debated. We aimed to determine whether sex-related differences exist in left ventricular mass index (LVMI), and myocardial mechano-energetic efficiency (MEEi) in with normal glucose tolerant (NGT), pre-diabetic and newly diagnosed type 2 diabetic subjects.MethodsSex-related differences in LVMI and myocardial MEEi, assessed by validated echocardiography-derived measures, were examined among 1562 adults with NGT, prediabetes, and newly diagnosed T2DM, defined according to fasting glucose, 2-h post-load glucose, or HbA1c.ResultsWorsening of glucose tolerance in both men and women was associated with an increase in age-adjusted LVMI and myocardial MEEi. Women with newly diagnosed T2DM exhibited greater relative differences in LVMI and myocardial MEEi than diabetic men when compared with their NGT counterparts. Prediabetic women exhibited greater relative differences in myocardial MEEi, but not in LVMI, than prediabetic men when compared with their NGT counterparts. The statistical test for interaction between sex and glucose tolerance on both LVMI (P < 0.0001), and myocardial MEEi (P < 0.0001) was significant suggesting a sex-specific association.ConclusionsLeft ventricle is subject to maladaptive changes with worsening of glucose tolerance, especially in women with newly diagnosed T2DM. The sex-specific increase in LVM and decrease in MEEi, both being predictors of CVD, may have a role in explaining the stronger impact of T2DM on the excess risk of CVD in women than in men.