P2488The 2013 ACC/AHA pooled cohort equations and insulin resistance status for detection of early-stage heart failure in the community

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
N Cauwenberghs ◽  
K Hedman ◽  
Y Kobayashi ◽  
F Haddad ◽  
T Kuznetsova

Abstract Objectives Detection of heart failure (HF) in its subclinical phase would allow timely initiation of preventive measures that counter its pathophysiology. Here, we assessed the usefulness of traditional cardiovascular (CV) risk assessment and insulin resistance status to detect early-stage HF. Methods In 984 participants (mean age, 57.0 years, 52.3% women), we derived echocardiographic indexes of left ventricular (LV) structure and function and calculated the 10-year risk for a first atherosclerotic CV disease (ASCVD) using the 2013 ACC/AHA risk score. We assessed the discriminatory value of this risk score to detect LV maladaptation and the improvements in reclassification by insulin resistance status (HOMA-IR). Results The probability for LV maladaptation rose progressively with the 10-year ASCVD risk increasing. Participants at high 10-year ASCVD risk (>7.5%) had indeed significantly higher odds for LV concentric remodeling (odds ratio, 4.84), LV hypertrophy (OR, 5.93), abnormal LV longitudinal strain (OR, 2.04) and LV diastolic dysfunction (OR, 25.3) as compared to those at low ASCVD risk (<2.5%; P≤0.0003). Adding markers of insulin resistance to the ACC/AHA risk score moderately improved the integrated discrimination and net reclassification of all LV maladaptive phenotypes (P≤0.022) except LV diastolic dysfunction (P≥0.059). LV remodeling and abnormal LS was particularly more likely in insulin-resistant participants with a 10-year ASCVD risk between 5% and 15% than in their insulin-sensitive counterparts. Prediction of early-stage HF profiles 2013 ACC/AHA risk score Addition of insulin resistance status to the 2013 ACC/AHA risk score AUC (95% CI) Integrated Discrimination Improvement Net Reclassification Improvement Absolute IDI (%) P value NRI (95% CI) P value LV concentric remodeling 0.70 (0.66 to 0.74) 0.0083 (11.3%) 0.022 0.23 (0.067 to 0.39) 0.0058 LV hypertrophy 0.70 (0.66 to 0.74) 0.017 (20.7%) 0.0033 0.27 (0.11 to 0.43) 0.0011 Abnormal LV LS 0.56 (0.53 to 0.62) 0.022 (202.0%) <0.0001 0.33 (0.18 to 0.49) <0.0001 LV diastolic dysfunction 0.82 (0.78 to 0.86) 0.0007 (0.45%) 0.84 0.093 (−0.11 to 0.30) 0.38 ≥2 LV abnormalities 0.76 (0.72 to 0.80) 0.0087 (7.3%) 0.071 0.22 (0.042 to 0.40) 0.016 The integrated discrimination improvement (IDI) and net reclassification improvement (NRI) reflect the improvements in classification by adding insulin resistance (by HOMA-IR) to the 2013 ACC/AHA risk score. HOMA-IR, Homeostatic Model for Assessment of Insulin Resistance; LS, longitudinal strain; LV, left ventricular. Risk enhancers of LV maladaptation Conclusions The 2013 ACC/AHA risk score adequately captured the risk for echocardiographic phenotypes of early-stage HF. As risk enhancer, insulin resistance might improve risk stratification of subclinical HF in subjects at intermediate risk. Acknowledgement/Funding The European Union, European Research Council and the Flanders Scientific Research Fund supported this study.

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Guanghong Jia ◽  
Brian P Bostick ◽  
Javad Habibi ◽  
Annayya R. Aroor ◽  
Vincent G. DeMarco ◽  
...  

Hyperuricemia is frequently observed in obese people and rising obesity rates parallel increased consumption of a high-fat/high-fructose western diet (WD). Epidemiologic and clinical data suggest that serum uric acid (UA) is positively associated with serum parathyroid hormone (PTH) and may be linked with left ventricular (LV) hypertrophy and LV diastolic dysfunction. Accordingly, we hypothesized that allopurinol, a potent xanthine oxidase (XO) inhibitor, would prevent development of LV diastolic dysfunction, independent of blood pressure, by reducing the levels of UA and PTH. Four week-old C57BL6/J male mice were fed a WD and water with 125mg/L allopurinol. After 16 weeks, we assessed levels of UA, XO activity, PTH, as well as diastolic function by cardiac MRI and cardiac ultrastructure by transmission electron microscopy (TEM). Body weight and fat composition were obtained along with HOMA -IR testing for insulin resistance. Allopurinol has been show to exert no effect on blood pressure. High resolution cardiac MRI revealed diastolic dysfunction with WD feeding that was prevented by allopurinol (LV diastolic relaxation time 35.3 ms for WD, 25.4 ms for CD and 27.7 ms for WD+ allopurinol, p value <0.01; Initial filling rate 0. 28 μl/ms for WD, 0.43 μl/ms for CD and 0.42 μl/ms for WD+ allopurinol, p value <0.05). Body weight, fat mass, and HOMA-IR were increased by WD feeding but not significantly improved by allopurinol. However, allopurinol markedly decreased the WD-induced increase in heart weight associated with activation of translational S6 kinase. TEM examination of myocardial ultrastructure revealed that WD induced remodeling changes with large mitochondria with disordered cristae and increased lysosomes. The ultrastructural changes were improved with treatment by allopurinol. Furthermore, allopurinol significantly inhibited both of plasma and urine UA levels and cardiac XO activity caused by WD. Interestingly , WD increased PTH levels which were decreased in parallel with reductions in uric acid with allopurinol. These findings support the notion that increased plasma levels of UA, in concert with elevated PTH, may play a key role in LV hypertrophy and associated LV diastolic dysfunction that result from consuming a WD high in fructose and fat.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
K Yanaka ◽  
H Akahori ◽  
T Imanaka ◽  
K Miki ◽  
N Yoshihara ◽  
...  

Abstract Background Left ventricular (LV) systolic dysfunction and heart failure (HF) in patients with lower extremity artery disease (LEAD) is associated with an increased risk for adverse events. However, relationship between long-term outcome in patient with LEAD and LV diastolic dysfunction remains unclear. Purpose The aim of this study was to assess the impact of LV diastolic dysfunction on long-term outcome in patients with LEAD. Methods Two hundred patients (male 66%, mean age 76±9 years) with preserved LV systolic function assessed by echocardiography (ejection fraction ≥50%) were enrolled from a single-center database between January 2013 to May 2015. Baseline LEAD was identified by ABI <0.9 or history of lower extremity revascularization. Diagnosis of LV diastolic dysfunction was based on the ASE/EACVI guidelines. The 3-year cumulative incidence of primary endpoint compared between LEAD patients with LV diastolic dysfunction than those without. The primary endpoint was a composite of cardiovascular death, myocardial infarction, stroke and hospitalization for HF during 3 years follow-up. Multivariate analysis was performed to determine whether LV diastolic dysfunction was independently associated with the primary endpoint. Results LV diastolic dysfunction was identified in 31%. The mean observation period was 32±21 months. The primary endpoint occurred more frequently in patients with LV diastolic dysfunction than those without at 3 years (30% vs 16%, P=0.02). There were no significant differences between 2 groups in the myocardial infarction (3% vs 3%, P=0.73) and stroke (3% vs 3%, P=0.55). Cardiovascular death (19% vs 7%, P=0.01) and hospitalization for HF (19% vs 7%, P=0.01) were significantly higher in patients with LV diastolic dysfunction. In multivariate analysis, LV diastolic dysfunction was an independent predictor for primary endpoint (HR=2.28, 95% CI 1.10–4.73, P=0.02) (Table) Predictor for primary endpoint Factors Univariate model Multivariate model Hazard ratio [95% CI] P value Hazard ratio [95% CI] P value Age 1.03 [0.98–1.08] 0.24 1.03 [0.98–1.08] 0.22 Chronic kidney disease 1.53 [0.77–3.07] 0.23 1.25 [0.60–2.58] 0.55 Coronary artery disease 1.08 [0.53–2.18] 0.84 1.18 [0.56–2.50] 0.65 Cerebrovascular disease 1.93 [0.74–5.02] 0.17 2.28 [0.86–6.05] 0.10 Critical limb ischemia 3.75 [1.68–8.37] <0.01 3.72 [0.56–2.50] <0.01 LV diastolic dysfunction 2.37 [1.18–4.74] 0.02 2.28 [1.10–4.73] 0.03 Conclusions LV diastolic dysfunction increased the risk for adverse events in patients with LEAD. Acknowledgement/Funding None


2019 ◽  
Vol 17 (2) ◽  
pp. 35-38
Author(s):  
Shyam Kumar BK ◽  
S.D. Bassi ◽  
Alok Kumar Sah ◽  
Devendra Acharya

Objectives: The Aim of this study to assess and analyze the echocardiographic changes in chronic kidney disease patients on maintenance hemodialysis. Material and methods: We Performed Prospective study of echocardiographic changes in chronic kidney disease (CKD) patients undergoing maintenance hemodialysis at our institute. We performed M-mode echocardiography in 80 CKD patients without obvious clinical evidence of coronary artery disease, Valvular heart disease, congenital heart disease. Data was collected from November 2018 to Nov 2019. Results: 80 Patients Undergoing Hemodialysis were included in our study, out of them Echocardiography finding shown LV dilation and diastolic dysfunction in 39 (48.75%), left ventricular hypertrophy (LVH) in 41 (51.25%), systolic dysfunction and pericardial effusion in 22 (27.5%) and 11 (13.75%) patients respectively. RWMA was present in 10% and Valvular calcification was seen in 5 patients. In sub-group of patients with Hb<10 gm%, LVH was present in 32 (78.05%) vs 9 (21.95%) in patient group with Hb ≥ 10 gm% (p <0.01). Other Sub Group of Patients with BP > 140/90mmhg, LVH Was Present in 34 (82.92%) vs 7 (17.08%) in patients group with BP< 140/90 mm hg (p=0.02). In both sub group p value for systolic dysfunction, RWMA & pericardial effusion is statistically not significant. Conclusion: LV diastolic dysfunction and hypertrophy were most common echocardiographic findings. There was statistically significant correlation between anemia and presence of LVH and positive correlation between presence of hypertension and LVH.  


2020 ◽  
pp. 1-9

Heart Failure with preserved Ejection Fraction (HFpEF) is a clinical syndrome in which patients have symptoms of Heart Failure (HF), such as dyspnea and fatigue, a Left Ventricular Ejection Fraction (LVEF) ≥ 50% and evidence of cardiac dysfunction as a cause of symptoms, such as abnormal Left Ventricular (LV) diastolic dysfunction with elevated filling pressures. Besides LV diastolic dysfunction, recent investigations suggest a more complex and heterogeneous pathophysiology, including systolic reserve abnormalities, chronotropic incompetence, stiffening of ventricular tissue, atrial dysfunction, secondary Pulmonary Arterial Hypertension (PAH), impaired vasodilatation and endothelial dysfunction. Unlike Heart Failure with Reduced Ejection Fraction (HFrEF), clinical trials over the years have not yet identified effective treatments that reduce mortality in patients with HFpEF. A database on use of carvedilol in a private cardiologist's practice was begun in 1997 and concluded at the end of 2018. We used this database to test the hypothesis that combining pharmacological interventions to address diastolic dysfunction (carvedilol), volume overload (spironolactone/eplerenone) and endothelial dysfunction (statins) with weight loss may benefit patients with HFpEF. We report analysis of 335 patients with HFpEF comprised of 61% female (mean age 74 ± 8) and 39% males (mean age 72 ± 7). Initial EF ranged between 50 and 77% with mean EF of 57 ± 6%. Only 15 patients were changed to metoprolol succinate, verapamil or diltiazem because of adverse side effects. Two hundred and twenty of the patients were in normal sinus rhythm when started on carvedilol, spironolactone/eplerenone and statin therapy with weight loss counseling. After 5 years, 191 patients were still on combination therapy, and only 31 (17%) had developed Atrial Fibrillation (AF). Compared to previous HFpEF trials reporting a 32% risk of developing atrial fibrillation after 4 years, our combination therapy significantly (p < 0.05) reduced the risk of developing AF over 5 years. Thus, irrespective of age and sex with comorbidities of type 2 Diabetes Mellitus (DM) and Chronic Kidney Disease (CKD), patients with HFpEF can be managed successfully with carvedilol, spironolactone/eplerenone and statins with a clinical benefit being a reduced risk of developing AF. We consider these data hypothesis-generating and hope these results will be tested further in database analyses and clinical trials.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Rebecca H Ritchie ◽  
Nga Cao ◽  
Yung George Wong ◽  
Sarah Rosli ◽  
Helen Kiriazis ◽  
...  

Nitroxyl (HNO), a redox congener of NO•, is a novel regulator of cardiovascular function combining vasodilator and positive inotropic properties. Our previous studies have demonstrated these properties occur concomitantly in the intact heart; HNO moreover also exhibits antihypertrophic and superoxide-suppressing actions. HNO donors may thus offer favorable actions in heart failure. The impact of chronic HNO donor administration has however yet to be reported in this context. We tested the hypothesis that the HNO donor 1-nitrosocyclohexyl acetate (1-NCA) limits cardiomyocyte hypertrophy and left ventricular (LV) diastolic dysfunction in a mouse model of diabetic cardiomyopathy in vivo. Male 6 week-old FVB/N mice received either streptozotocin (55 mg/kg/day i.p. for 5 days, n=17), to induce type 1 diabetes, or citrate vehicle (n=16). After 4 weeks of hyperglycemia, mice were allocated to 1-NCA therapy (83mg/kg/day i.p.) or vehicle, and followed for a further 4 weeks. As shown in the table, blood glucose was unaffected by 1-NCA. LV diastolic dysfunction was evident in diabetic mice, measured as echocardiography-derived A wave velocity, deceleration time and E:A ratio; LV systolic function was preserved. Diabetes-induced diastolic dysfunction was accompanied by increased LV cardiomyocyte size, hypertrophic and pro-fibrotic gene expression, and upregulation of LV superoxide. These characteristics of diabetic cardiomyopathy were largely prevented by 1-NCA treatment. Selectivity of 1-NCA as a donor of HNO versus NO• was demonstrated by the sensitivity of the coronary vasodilation response of 1-NCA to the HNO scavenger L-cysteine (4mM), but not to the NO• scavenger hydroxocobalamin (50μM), in the normal rat heart ex vivo (n=3-7). Collectively, our studies provide the first evidence that HNO donors may represent a promising new strategy for the treatment of diabetic cardiomyopathy, and implies their therapeutic efficacy in settings of chronic heart failure.


2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Elisa Tomarelli ◽  
Federica Moscucci ◽  
Anna Annunziata Losardo ◽  
Pellegrina Pugliese ◽  
Mauro Schina ◽  
...  

Abstract Aims Complications associated with iron accumulation were highly recurrent in thalassemia patients, who underwent frequent blood transfusions, in particular hemosiderotic cardiomyopathy which could lead to heart failure and arrhythmias. Nowadays, the better iron chelation therapy has improved cardiovascular morbidity in these patients; nevertheless, mild impairment should be seek for and eventually treated. The objective of our study was to evaluate the possibility of using early electrocardiographic markers of myocardial damage and predictors of mortality, such as the Electric Risk Score (ERS). Methods and results 73 patients with thalassemia major were enrolled in this study, which were divided into two groups, with 45 years old as cut off. Anamnestic, clinical, electrocardiographic, and echocardiographic data were collected. From ECG, ERS was obtained. over 45 yrs-old group of pts, in addition to a predictable increase in the prevalence of traditional cardiovascular risk factors and drug intake, an alteration of the QRS-T angle (14[30] vs. −4[28], p value: &lt;0.0001) and an increased prevalence of left ventricular hypertrophy (2.88 ± 0.86 vs. 2.40 ± 0.57 p value: &lt;0.05) were found. In patients taking drugs with possible interactions with the ventricular repolarization phase, there is a slight increase in the QT interval, left ventricular hypertrophy and a reduction in Tpeak-Tend (Table 1). Electrocardiographic values in groups of patients with different age groups who are taking therapies that can affect QT. The echocardiogram revealed an increase in the end-diastolic diameter of the right ventricle (26 ± 3 vs. 28 ± 3 mm, P-value: 0.05) in the group of patients over the age of 45, a decrease in the acceleration time of the pulmonary systolic flow (138 ± 25 vs. 125 ± 13 ms, P-value: 0.04) and TAPSE (25 ± 3 vs. 22 ± 4 mm, P-value: 0.002). Conclusions From the data in our study it emerged that an appropriate iron-chelation therapy is able to effectively counteract the hemosiderotic cardiomyopathy of thalassemic patients so as to detect electro- and echocardiographic anomalies only in patients of more advanced age, a result that we think both the consequence, not so much of iron overload, but of an increase in the prevalence of age- and gender-related cardiovascular risk factors. The initial changes in cardiac electromechanics, which can be assessed with the aforementioned methods, we believe, can become a very early sign of specific myocardial damage. 329 Figure 1Electrical risk score parameters.


Author(s):  
Swapnil Jain ◽  
C. L. Nawal ◽  
Amandeep Singh ◽  
Radhey Shyam Chejara ◽  
Sagar Barasara ◽  
...  

Background: Diastolic dysfunction in patients suffering from diabetes mellitus represents an earlier stage in the natural history of cardiomyopathy. This study was done to assess the left ventricular diastolic dysfunction in recently diagnosed (<5yr) Type 2 Diabetes Mellitus by Echocardiography and also to determine association of glycemic status (by HBA1c levels) with left ventricular diastolic dysfunction (LVDD).Methods: An observational descriptive study involving 100 diabetic patients, taken on first come first serve basis after applying inclusion and exclusion criteria. In all the subjects, other than routine investigations, HbA1c was estimated and echocardiography was done to evaluate LVDD.Results: Mean value of HbA1c in the study was 8.31+ 1.408 %. 63 out of 100 subjects had LVDD. There was significant positive correlation between HbA1c and LVDD (p value <0.001). As HbA1c increased, severity of LVDD increased. In this study, as BMI increased, HbA1c and LVDD increased & both findings were statistically significant (p value =0.001).Conclusion: Our study indicates that myocardial damage in patients with diabetes affects diastolic function before systolic function &higher HbA1C level is strongly associated with presence of LVDD. Patients should be advised strict control of diabetes in order to reduce the risk for developing LVDD which is a precursor for more advanced disease.Keywords: Diabetes mellitus, Diastolic dysfunction, BMI, HbA1c


2006 ◽  
Vol 290 (3) ◽  
pp. H1064-H1070 ◽  
Author(s):  
Shinsuke Kido ◽  
Naoyuki Hasebe ◽  
Yoshinao Ishii ◽  
Kenjiro Kikuchi

The aim of this study was to investigate what factor determines tachycardia-induced secretion of atrial and brain natriuretic peptides (ANP and BNP, respectively) in patients with hypertrophic cardiomyopathy (HCM). HCM patients with normal left ventricular (LV) systolic function and intact coronary artery ( n = 22) underwent rapid atrial pacing test. The cardiac secretion of ANP and BNP and the lactate extraction ratio (LER) were evaluated by using blood samples from the coronary sinus and aorta. LV end-diastolic pressure (LVEDP) and the time constant of LV relaxation of tau were measured by a catheter-tip transducer. These parameters were compared with normal controls ( n = 8). HCM patients were divided into obstructive (HOCM) and nonobstructive (HNCM) groups. The cardiac secretion of ANP was significantly increased by rapid pacing in HOCM from 384 ± 101 to 1,268 ± 334 pg/ml ( P < 0.05); however, it was not significant in control and HNCM groups. In contrast, the cardiac secretion of BNP was fairly constant and rather significantly decreased in HCM ( P < 0.01). The cardiac ANP secretion was significantly correlated with changes in LER ( r = −0.57, P < 0.01) and tau ( r = 0.73, P < 0.001) in HCM patients. Tachycardia potentiates the cardiac secretion of ANP, not BNP, in patients with HCM, particularly when it induces myocardial ischemia and LV diastolic dysfunction.


2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Lewis Ari Eisen ◽  
Pericles Davlouros ◽  
Dimitrios Karakitsos

Heart failure with a normal or nearly normal left ventricular (LV) ejection fraction (HFNEF) may represent more than 50% of heart failure cases. Although HFNEF is being increasingly recognized, there is a relative lack of information regarding its incidence and prognostic implications in intensive care unit (ICU) patients. In the ICU, many factors related to patient’s history, or applied therapies, may induce or aggravate LV diastolic dysfunction. This may impact on patients’ morbidity and mortality. This paper discusses methods for assessing LV diastolic function and the feasibility of their implementation for diagnosing HFNEF in the ICU.


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