Ультрасоноґрафічна характеристика структури і функції серця у хворих із синтропічною кардіоміопатією на ґрунті цирозу печінки та їх особливості залежно від тяжкості основної хвороби

475 Larger left ventricle size negatively impacts late postoperative left ventricle function following mitral valve repair

Purpose of the study. Comparative evaluation of echocardiographic and morphometric dimensions of the rat heart left ventricle. Materials and methods. The study included 10 outbred male rats weighing 160–180 g. The size of the heart left ventricle was assessed using echocardiography and morphometry. The measurements were carried out according to standard protocols. To perform morphometric measurements, hearts were stopped in systole with a lethal dose (1.0 mg/kg) of 0.025 % strophanthin K solution, and in diastole, by immersing the hearts in a chilled physiological solution (calcium-free medium). Results. It was shown that the systolic size of the left ventricle of the heart according to echocardiography is 1.79Ѓ}0.10 mm, and morphometry 1.64Ѓ}0.09 mm (p = 0,302); diastolic size of the left ventricle, respectively, 3.42Ѓ}0.16 mm and 3.66Ѓ}0.17 mm (р = 0,318). The detected discrepancies do not exceed 10 % and, apparently, are due to the fact that the physiological dimensions of the heart left ventricle are measured by a non-invasive echocardiographic method, and for morphometric measurements of the dimensions in the systole, the heart was stopped by injection of strophanthin K, which entails an overload of heart cells with Ca2+ ions and as a result, contracture of cardiomyocytes; post-mortem cardiac arrest in diastole, in a calcium-free environment, is accompanied by a loss of cardiac muscle tone and, therefore, dilatation of the left ventricle will naturally be greater than physiological. Conclusion. Noninvasive echocardiographic measurement of the size of the heart left ventricle fully reflects the actual size of the left ventricle of the rat heart (the difference does not exceed 10 %), i. e. echocardiographic measurements are valid.

Pulmonary artery pressure and diastolic dysfunction in normal left ventricular systolic function

The prevalence of cirrhotic cardiomyopathy is an issue hard to estimate, both nationally and worldwide. This clinical research sets out a more precise evaluation of systolic and diastolic functions in cirrhotic patients using proven parameters - the TEI Index- to estimate systolic and diastolic dysfunction and the E/Vp ratio for diastolic dysfunction. These parameters were compared with classic parameters typically employed. The study population was represented by 70 patients diagnosed with liver cirrhosis. Results showed increased sensitivity of the TEI Index - in detecting systolic dysfunction in cirrhotic patients, with an increased accuracy compared to left ventricular ejection fraction. Regarding the parameters for diastolic dysfunction, it was proved that the E/Vp ratio had an increased specificity in detecting diastolic dysfunction due to cirrhotic cardiomyopathy. In conclusion, the hypothesis that patients with liver cirrhosis could benefit from an improvement in diagnostic sensitivity of cirrhotic cardiomyopathy using the two suggested parameters was confirmed in our study. And more important, a significant positive correlation between the severity of diastolic dysfunction and the severity of liver disease was found.

Heart failure with preserved ejection fraction (HFpEF) accounts for more than 50% of all HF cases. HFpEF patients manifest normal or mildly reduced left ventricle (LV) ejection fraction (LVEF), LV hypertrophy, diastolic dysfunction, myocardial stiffness, cardiac fibrosis, hypertension, nephropathy and sudden death. There is no appropriate animal model for HFpEF. The Alport Col4a3 -/- mouse, a model of nephropathy, hypertension and early death, develops a cardiovascular pathology that is yet to be well characterized. We elected to analyze the cardiovascular pathology of the Alport mouse and investigate any commonalities with HFpEF. Male Alport and wild type (WT) littermates of mixed background at 2 months of age were subjected to echocardiographic and 2D speckle tracking analyses and heart tissues were used for histopathological examinations (N=6 mice per group). Circulating Galectin-3, a marker of HFpEF, was measured by Elisa in plasma samples. Data are shown as mean±SEM. Normalized heart weight increased in Alport relative to WT mice - p<0.01, indicative of cardiac hypertrophy. Consistently, echocardiography showed interventricular septum (IVS) thickening -p<0.05. Reduced stroke volume p<0.01, and impaired global longitudinal and circumferential strain (GLS and GCS) indicated systolic dysfunction in Alport mice. No significant reduction in LVEF was observed. Alport mice developed diastolic dysfunction evidenced by a prolonged Isovolumetric relaxation time -P<0.05, and a reduced E/A, a marker of LV relaxation and stiffness -p<0.01. Elevated LV filling pressure and pulmonary artery wedge pressure were demonstrated by an increase in E/E’ - p<0.01. Galectin-3 increased in Alport relative to WT plasma (P<0.01). Alport hearts had more Fibronectin protein - P<0.05 and increased number of fibroblasts with “activated” phenotype as demonstrated by increased mass of rough endoplasmic reticulum in EM cross sections. Our study suggests that the cardiovascular pathologies of the Alport mouse are similar to HFpEF, specifically preserved ejection fraction, diastolic dysfunction, hypertension, early death and cardiac stiffness and fibrosis. Further study of this multi-factorial pathology may render the Alport mouse as a useful novel model for HFpEF.

Chronic primary mitral regurgitation (MR) exposes the left ventricle (LV) to volume overload and is associated with evidence of fibrosis on non-invasive imaging. It is not known whether fibrosis predicts outcome from surgery. This study aimed to 1) quantify myocardial fibrosis on histology and non-invasive imaging, 2) investigate any association between fibrosis and LV size and function, 3) determine the impact of fibrosis on post-operative outcome. Methods In a prospective observational multicentre study, 105 patients with severe MR (N=65/32/8 NYHA Class I/II/III respectively; mean age 63.1±13.4 years; male 73%; VO2max 91.2±22.4%) had multiparametric cardiac magnetic resonance (CMR), symptom assessment (Minnesota Living with Heart Failure Questionnaire (MLHFQ)) and cardiopulmonary exercise testing before and at 9 months following repair. Patients consented for up to 3 intraoperative LV biopsies for histological collagen volume fraction (CVF) quantification. Results 234 LV biopsies were feasible from 86 patients with median CVF of 14.6% [IQR 7.4–20.3]. Fibrosis was present even in NYHA Class I patients (13.6% [6.3–18.8]), and was significantly higher than the 3.3% [2.6–6.1] obtained from 8 autopsy controls without cardiac disease (P<0.001). Pre-operatively, there was no relationship between CVF and LV size, systolic function, ECV, late gadolinium enhancement, although it did correlate with MLHFQ (R=0.23, P=0.034). Conversely, ECV (27.4±3.3%) correlated with systolic (LVEF Rho=−0.22, P=0.029; LVESVi Rho=0.22, P=0.025, GCS Rho=0.31, P=0.002) and diastolic function (E/e' R=0.25, P=0.022), exercise capacity (%VO2max R=−0.22, P=0.030), with borderline correlation to MLHFQ (R=0.19, P=0.058). Post-operatively, although LVEF remained normal (defined as >50%) in all but 6 patients (LVEF pre 69.1±8.0 vs post 63.3±8.3%, P<0.001), there was a reduction in ECV (27.4±3.3 vs 26.6±2.8%, P=0.027) that was proportionate to its pre-operative expansion (Figure1), suggesting that fibrosis was reversible within our patients. Neither histological CVF nor ECV predicted change in LVESVi, LVEF, symptom burden or exercise capacity following repair. GCS was an independent predictor of post-operative LVESVi and LVEF on multiple linear regression models. Whilst improvements in symptom burden and exercise capacity was observed in NYHA II-III patients, this sub-group of patients failed to achieve the same level of fitness and symptom-free status as NYHA I patients (VO2max 92.2±18.8% vs 102.9±21.1%, P=0.017; MLHFQ 12 [5–26] vs 3 [0–10], P<0.001). Conclusions Myocardial fibrosis is present in primary MR, before the onset of symptoms. Due to its patchy nature, ECV but not fibrosis on histology is a better marker of pre-operative myocardial function and symptom status. Despite ECV reduction following successful MR surgery, symptomatic patients fail to regain exercise fitness and symptom-free status – providing further support for the benefits of early surgery. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): British Heart Foundation

BackgroundLeft ventricular diastolic dysfunction is associated with mortality outcomes in severe sepsis and septic shock. There are ongoing issues with diagnosing diastolic dysfunction in this cohort, partly owing to the poor applicability of traditional parameters in the hyperdynamic circulation. In this feasibility study, we sought to assess the utility of a novel parameter (septal e′/s′) to identify diastolic dysfunction in patients with severe sepsis and septic shock who had normal systolic function against the 2016 American Society Echocardiography and European Association of Cardiovascular Imaging (ASE/EACI) guidelines on diastolic dysfunction.MethodsIn this prospective observational pilot study, patients identified as having severe sepsis and septic shock underwent transthoracic echocardiography on day 1 and day 3 of their intensive care unit admission. In patients with normal systolic function, septal e′/s′ was calculated using the peak modal velocity of the s′ compared with the e′ from the septal annulus tissue Doppler imaging and compared with their diastolic grade according to the 2016 ASE/EACI guidelines on diastolic dysfunction.ResultsOn day 1 of admission, 44 of 62 patients with severe sepsis and septic shock had normal systolic function. There was a strong association of those with diastolic dysfunction having a reduced septal e′/s′ compared with patients with normal diastolic function (AUC 0.91). A similar relationship was seen with patients who had indeterminate diastolic dysfunction. On day 3, 37 patients had normal systolic function. Again, there was a strong association of those with diastolic dysfunction and a reduced septal e′/s′ (AUC 0.95).ConclusionsA reduction in septal e′/s′ may indicate diastolic dysfunction in patients with severe sepsis and septic shock who have normal systolic function. As opposed to limited traditional measures of diastolic dysfunction, it is applicable in those with hyperdynamic systolic function.

Chronic primary mitral regurgitation (MR) exposes the left ventricle (LV) to volume overload and is associated with evidence of fibrosis on non-invasive imaging. It is not known whether fibrosis predicts...

Characterization of atrial histology in a patient with hypertrophic cardiomyopathy: Possible evidence of a primary atrial myopathy

Heart failure with preserved ejection fraction (HFpEF) (diastolic heart failure) is a clinical syndrome that now accounts for at least half the cases of heart failure in adult patients. Decompensated HFpEF is a common and costly reason for admission to the hospital.1 From a pathophysiologic perspective, the left ventricle (LV) is stiff or noncompliant and characterized by an altered pressure-volume relationship.2 Asymptomatic LV diastolic dysfunction is a precursor to this clinical heart failure syndrome, and obesity and hypertension are the major risk factors for both diastolic dysfunction and HFpEF. Patients with early-stage HFpEF are characterized by euvolemic dyspnea.3 As the syndrome advances, congestion and atrial fibrillation develop. In late stages, pulmonary hypertension and the cardiorenal syndrome are common. The clinical course often results in recurrent hospital admissions for decompensated heart failure. Guideline-directed medical and device therapy, often beneficial for patients with heart failure with reduced ejection fraction (systolic heart failure), does not exist for patients with HFpEF. Decongestion is usually the only therapeutic option for patients with decompensated HFpEF, but diuresis can prove difficult in patients with the cardiorenal syndrome. Caring for such patients is frustrating and difficult.Why would a pediatrician care about a heart failure syndrome in adults? Because obesity and inactivity during childhood may lay the foundation for HFpEF in adulthood. In this issue of Pediatrics, Heiskanen et al4 report on the relationship between cardiovascular risk factors in children and left ventricular diastolic dysfunction in adulthood. The Cardiovascular Risk in Young Finns Study (YFS) was an ambitious multicenter longitudinal study of cardiovascular risk factors from childhood to adulthood in the general population of Finland. The baseline study was conducted in 1980 and included 3596 children and adolescents (51% female participants). Follow-up data were collected in 1983, 1986, 1989, 2001, 2007, and 2011. Echocardiography was performed on 1994 of the participants in 2011 (ages 34–49 years). Using a clinically accepted noninvasive Doppler-derived assessment of LV diastolic function and LV filling pressure (mitral E/e′ ratio [E: velocity of early diastolic filling of the LV; e′: velocity of the mitral annulus during diastole]), the authors identified 3 major childhood risk factors that were associated with diastolic dysfunction in adulthood: increased childhood adiposity, decreased physical activity, and increased systolic blood pressure.4,5 The associations of childhood adiposity and physical activity with adult diastolic dysfunction were independent of adulthood levels of the same factors, whereas childhood systolic blood pressure was not.The YFS suggests that, in some patients, LV myocardial structural changes may start decades before the onset of the clinical heart failure syndrome we call HFpEF. Over the years, millions of dollars have been spent on negative clinical trials looking for the “holy grail” of HFpEF treatment. In reality, it is unrealistic to think that a drug is going to reverse structural changes that started decades before drug treatment commenced.What, then, is the answer to HFpEF? Prevention. Given the results of the YFS, prevention should begin during childhood. Focusing on prevention early should result in a reduced burden of HFpEF as well as other medical problems commonly seen in adults. Where do we start? In 2010, the American Heart Association defined national goals for cardiovascular health promotion and disease reduction for children and adults.6 This gave rise to My Life Check Life’s Simple 7. The Simple 7 included the following: manage blood pressure, control cholesterol, reduce blood sugar, get active, eat better, lose weight, and stop smoking.7 The Simple 7 outlines a comprehensive way to improve one’s health and reduce cardiovascular risk for children and adults. But implementing 7 actionable items is difficult for most individuals, especially children. Rather than the Simple 7, for children, I would start with the Terrific 2: increased physical activity and sodium restriction. Implementing these 2 actionable items is far simpler than 7 and should result in reduced rates of obesity and hypertension in adulthood.Right now, adult cardiologists are overwhelmed by the sheer volume of patients with HFpEF and frustrated by the lack of treatment options. One day, it would be nice to ask what happened to all of the patients with HFpEF. Although the Simple 7 are more comprehensive, adoption of the Terrific 2 is a step toward the lofty but achievable goal of decreasing the number of adults with HFpEF and other cardiovascular problems.

Perioperative Transthoracic Echocardiography: “Universal Acid”?

Is ‘diastolic heart failure’ a diagnosis of exclusion? Echocardiographic parameters of diastolic dysfunction in patients with heart failure and normal systolic function

Repair of Infracardiac Total Anomalous Pulmonary Venous Return

In recent years surgical closure of defects in the ventricular septum has become a beneficial and relatively safe procedure. This increase in the scope of cardiac surgery demands specificity not only in establishing an accurate anatomic diagnosis but also in evaluating the associated hemodynamic alterations. One must be able to predict whether surgical closure of the anatomic defect will result in improvement or deterioration of the cardiac status. There appears to be no unanimity of opinion among thoracic surgeons in regard to the criteria of operability for patients with ventricular septal defects and severe pulmonary hypertension. At the Mayo Clinic the decision as to operability has become increasingly dependent on the magnitude of the pulmonary artery flow, which is considered to be a reflection of the degree of resistance in the pulmonary vascular bed (3). It was the purpose of the study to be reported here to evaluate the role of conventional roentgen methods in estimating this flow in the presence of a ventricular septal defect. Funtional Pathology of Ventricular Septal Defect A defect may occur in either the muscular or the membranous portion of the ventricular septum, but is found more commonly in the membranous portion which forms the superior part of the septum. Of more significance than the location of the defect is its size. In small defects (maladie de Roger), the normal differential pressure between the right and left ventricles is maintained and the magnitude of the arteriovenous shunt through the defect is not clinically significant. If the defect is large, however, the differential pressure between the ventricles is not maintained and the resultant arteriovenous shunt may be 50 per cent or more of the left ventricular output. The consequent increase in the volume of blood and velocity of flow into the lesser circulation produces changes in the pulmonary vascular tree which may be recognized readily on the conventional postero-anterior roentgenogram of the thorax (2, 6, 7) (Figs. 1–4). These changes are usually manifested as an increase in the size of the main pulmonary artery and its branches, enlargement of both ventricles, and an associated hypoplastic aortic arch. Fluoroscopy shows vigorous pulsations of the central (hilar) branches of the pulmonary artery. Ventricular septal defect is more frequently associated with pulmonary arterial hypertension than are most other cardiac anomalies. The hypertension may be due to two factors (4): (a) It may be the result of the increase in volume and velocity of blood entering the pulmonary circulation in the presence of normal pulmonary vascular resistance. Since the pulmonary resistance is normally about a fifth of that in the systemic vascular bed, the arteriovenous shunt through any considerable defect is rather large and consequently the pulmonary artery flow is greatly increased.

The potential benefits of fetal cardiac intervention (FCI) have been realized for many years. In 1975, Eibschitz et al1 reported intrapartum treatment of fetal ventricular tachycardia by administering propranolol to the mother, and as early as 1986, in utero pacing was attempted for complete heart block in a human fetus.2 Recently, however, interest in FCI has accelerated.3–18 As with other fetal interventions,19,20 FCI can only become a highly useful clinical tool if it is applied to conditions in which a feasible mode of therapy is available and either the fetus is at risk for demise as a result of the condition or intervention may alter the evolution of the condition such that the severity of the postnatal disease is substantially reduced (Table 1). For conditions in which the fetus is at high risk for prenatal or neonatal death, the rationale for FCI is obvious, to improve survival. If death is not imminent but the disease is likely to have major lifelong morbidity, the rationale is that FCI will modify the course of cardiac growth, function, and/or development in utero sufficiently to alter postnatal outcome and justify the potential risks of the procedure. Prenatal intervention may also allow the fetus to recover in the supportive in utero environment, during a developmental period when there is enhanced wound healing and the capacity for myocyte proliferation.21,22 View this table: Table 1. Congenital Cardiovascular Anomalies Potentially Amenable to FCI This construct rightfully emphasizes death or significant morbidity as therapeutic targets. FCI can entail substantial short-term risk to the fetus, uncertain long-term risk to the fetus and child, and at least some risk to the mother. There are no known medical benefits to the mother. With that risk profile, FCI will not be embraced by the maternal-fetal medicine and cardiology communities unless it …