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 Table of Contents  
ORIGINAL ARTICLE
Year : 2013  |  Volume : 23  |  Issue : 4  |  Page : 96-101

Asymptomatic left ventricular dysfunction and metabolic syndrome: Results from an Italian multicenter study


1 Internal Medicine, A.O.R. Villa Sofia Cervello, Palermo, Italy
2 Cardiology, University of Messina, Messina, Italy
3 Cardiology, Hospital S. Maria degli Angeli, Pordenone, Italy
4 Cardiology, University of Catania, Catania, Italy
5 Cardiology, Monaldi Hospital, Naples, Italy
6 Cardiology, Policlinic of Bari, Bari, Italy
7 Italian Society of Cardiovascular Echography, Milan, Italy
8 Cardiology, Hospital of Reggio Calabria, Reggio di Calabria, Italy
9 Cardiology, University of Pisa, Pisa, Italy

Date of Web Publication20-Feb-2014

Correspondence Address:
Salvatore La Carrubba
Medicina Interna - Azienda Ospedali Riuniti Villa Sofia Cervello - Palermo, Piazzetta Salerno, 1 - 90100 Palermo
Italy
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Source of Support: None, Conflict of Interest: Declared.


DOI: 10.4103/2211-4122.127410

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  Abstract 

Context: Metabolic syndrome (MS) is a cluster of interrelated common clinical disorders, including obesity, insulin resistance, glucose intolerance, hypertension and dyslipidemia, associated with a greater risk of atherosclerotic cardiovascular disease than any of its individual components. Although MS is associated with increased cardiovascular risk (CVR), its relationship with heart failure (HF) and left ventricular (LV) dysfunction is not fully understood. Aims: We sought to determine whether MS is associated to LV systolic and diastolic dysfunction in a sample of patients with MS and no symptoms for HF. Subjects and Methods: We enrolled 6422 consecutive asymptomatic patients admitted to echo-lab for a routine echocardiogram. We calculated LV systolic and diastolic function, by Simpson biplane method and validated Doppler parameters, respectively. MS was diagnosed if three or more CVR factors were found. Results: LV systolic function was evaluated in 6175 patients (96.2%). In the group of patients without MS (n = 5630), the prevalence of systolic dysfunction was 10.8% (n = 607) while in the group of patients with MS (n = 545) it was 12.5% (n = 87), (RR1.57; CI 95% 1.2-2.0; P < 0.001). Diastolic function was evaluated in 3936 patients (61.3%). In the group of patients without MS (n = 3566) the prevalence of diastolic dysfunction was 33.3% (n = 1187), while in patients with MS (n = 370) it was 45.7% (n = 169), (RR1.68; CI95% 1.3-2.0; P < 0.001). After adjustment for age and gender, MS proved to be an independent predictor of LV systolic and diastolic dysfunction. Conclusions: Our data show that asymptomatic LV systolic and diastolic dysfunction, is correlated with MS and demonstrate that echocardiography is a useful tool to detect patients at high risk for HF. Echocardiography in asymptomatic patients with MS may lead to a therapy initiation at early stages to prevent future cardiovascular events and HF.

Keywords: Diastolic ventricular dysfunction, echocardiography, metabolic syndrome, systolic ventricular dysfunction


How to cite this article:
La Carrubba S, Todaro MC, Zito C, Antonini-Canterin F, Monte IP, Caso P, Colonna P, Gregorio C, Pezzano A, Benedetto F, Salvo GD, Carerj S, Bello VD. Asymptomatic left ventricular dysfunction and metabolic syndrome: Results from an Italian multicenter study. J Cardiovasc Echography 2013;23:96-101

How to cite this URL:
La Carrubba S, Todaro MC, Zito C, Antonini-Canterin F, Monte IP, Caso P, Colonna P, Gregorio C, Pezzano A, Benedetto F, Salvo GD, Carerj S, Bello VD. Asymptomatic left ventricular dysfunction and metabolic syndrome: Results from an Italian multicenter study. J Cardiovasc Echography [serial online] 2013 [cited 2019 Mar 21];23:96-101. Available from: http://www.jcecho.org/text.asp?2013/23/4/96/127410


  Introduction Top


Congestive Heart failure (HF) is classified according to clinical and instrumental findings into four stages. Stage A and B being the first two are characterized by the presence of clinical risk factors and structural abnormalities, respectively, asymptomatically. [1],[2]

These silent abnormalities may lead over a time to symptomatic left ventricular dysfunction (LVD) (stage C and D). [3],[4],[5],[6] Early detection of subclinical form of LVD may lead to establish an early protective treatment and potentially delay the development into overt HF. [7],[8] Metabolic syndrome (MS) is a cluster of several risk factors for cardiovascular diseases associated with an higher incidence of symptomatic HF and cardiovascular events. [9],[10],[11],[12] Data from Third National Health and Nutrition Examination Survey (NHANES III) showed that patients with MS had nearly twice the likelihood of self-reported HF, suggesting that MS may serve as a surrogate indicator for the association between insulin resistance and HF. [13] Moreover, each individual marker of MS is inferior to MS itself in identifying subtle cardiac dysfunction. [14] However, the prevalence of asymptomatic LV systolic and/or diastolic dysfunction is not well established in patients with MS at stage A or B of HF.

Aim of this study is to evaluate left ventricular systolic and/or diastolic abnormalities in a large sample of patients with MS and without symptoms of HF.


  Subjects and Methods Top


Study population

Total of 6422 consecutive patients (median age 59 years, interquartiles range: 48-68; men 3364) referred for a routine transthoracic examination to 75 national echocardiographic laboratories, were enrolled in the study. All laboratories were selected according to the competence level of the operators, which is level 3 in agreement with the American Society of Echocardiography (ASE) requirements. [15] Detailed history of all the patients were taken, with focus on cardiovascular risk factors. Exclusion criteria were: Dyspnoea, valvular heart disease at least of moderate degree, previous valvular heart surgery, coronary artery by-pass surgery within the previous six months.

In this study, we adopted the main definition of MS in accordance with the American Heart Association (AHA)/National Heart, Lung, and Blood Institute (NHLBI) scientific statements. [16] We diagnosed MS with the presence of at least three of the following: Hypertension, dyslipidemia, glucose intolerance and obesity with cutoff points consistent with the National Cholesterol Education Program's Adult Treatment Panel III (ATP III) report, modified with body mass index (BMI) in place of waist circumference. [12]

Hypertension was defined as systolic BP ≥ 140 mm Hg, diastolic BP ≥ 90 mm Hg, or self-reported antihypertensive medication use during the 2-week period before the clinical examination. [17] Dyslipidemia was defined as a low HDL cholesterol level ( < 40 mg/dL in men and < 50 mg/dL in women) or as an elevated triglyceride level ( ≥ 150 mg/dL). [18] Glucose intolerance was defined by the presence of diabetes (self-reported physician diagnosis of diabetes, use of insulin or oral hypoglycemic medication, or fasting glucose level ≥ 126 mg/dL) or impaired fasting glucose (fasting glucose level ≥ 110 mg/dL) according to American Diabetes Association criteria. [19] Subjects having three or more of the above mentioned criteria were classified as having MS.

Consistently with other major studies, we used BMI because we could not obtain waist circumference measurements for the entire study sample. [20],[21] The waist circumference criteria used in the ATP III definition were replaced with cutoff points for BMI (28.8 kg/m 2 for men and 26.7 kg/m 2 for women), as in previous studies. [22]

All patients underwent physical examination, 12-lead electrocardiography, and a complete transthoracic echocardiographic examination, according to the standardized protocol based on the recommendations of the ASE. [23]

Echocardiograms were analyzed when at least 80% of the endocardium was visible. Quantitative analysis was performed for each laboratory, by the same expert operator. Measurements of left ventricular ejection fraction (LVEF) were performed using the modified biplane Simpson's rule as a mean of three cardiac cycles. In patients with atrial fibrillation, the average value was obtained from six cardiac cycles. Left ventricular diastolic function was evaluated by measuring mitral valve and pulmonary venous flow Doppler parameters; the mitral flow was recorded in basal condition and during valsalva manoeuvre, according to the standard criteria. [24] The following echocardiographic parameters were evaluated: LVEF, mitral inflow [E wave velocity, A wave velocity, E/A, Δ E/A (changes from basal to valsalva manoeuvre), E wave deceleration time (DT), A wave duration (A dur )], pulmonary venous flow [(systolic velocity (S), diastolic velocity (D), a reverse wave duration (AR dur )].

Systolic LVD was defined as LVEF equal or less than 50%. [24] Diastolic function was classified, according to the progression of dysfunction, as follows: Normal (0.75 < E/A < 1.5, DT > 140 msec, ΔE/A < 0.5 during Valsalva manoeuvre, S ≥ D, AR dur < A dur ); mild (E/A≤0.75, DT > 140 msec, ΔE/A < 0.5, S > D, AR dur < A dur ); moderate (0.75 < E/A < 1.5, DT > 140 ms, ΔE/A ≥ 0.5, S < D or AR dur > A dur + 30 ms) and severe dysfunction (E/A > 1.5, DT < 140 ms, ΔE/A ≥ 0.5, S < D or ARdur > Adur+30 ms). [24] Participants were required to have at least two concordant Doppler criteria to be classified and patients with atrial fibrillation were excluded from evaluation of diastolic dysfunction.

The study was approved by the local research ethic committees and all patients gave a written informed consent.

Statistical analysis

All analyses were performed by using SPSS for Windows (version 12.0.1, Chicago Ill). Continuous variables are expressed as mean ΁ SD or as median and 25 th through 75 th interquartiles when appropriate. The association between age and presence of MS was evaluated using nonparametric Mann-Whitney U test. Categorical variables were compared by the chi-square test. Stepwise logistic regression analysis was used to determine the association between MS and left ventricular systolic and diastolic dysfunction adjusting for age and gender. A two-tailed P value of < 0.05 was considered significant.


  Results Top


A total number of 6422 patients were eligible for the study. Clinical characteristics of patients are shown in [Table 1]. Patients were divided according to the absence or presence of MS into Group A and Group B [Table 2]. Prevalence of MS was higher in man (9.1%) than in women (8.5%), but not statistically significant (P = 0.37).
Table 1: Study population characteristics


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Table 2: Risk factors and MS prevalence


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Left ventricular systolic function was evaluated in 6175 patients (96.2%); in the remaining 247 patients (3.8%) LVEF was not calculated because of poor acoustic window. In the group of patients with MS (group B), the prevalence of systolic dysfunction was significantly higher than in patients without MS (group A), 12.5% vs 10.8% (RR 1.57; CI 95% 1.2-2.0; P < 0.001) [Table 3].
Table 3: Systolic left ventricular dysfunction (LVD) in the two groups


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Diastolic function was evaluated in 3936 patients (61.3%). The overall prevalence of diastolic LVD was 33.3% (n = 1187) and was significantly higher in patients with MS, 45.7% vs 33.3% (RR 1.68; CI 95% 1.3-2.0; P < 0.001) [Table 4].
Table 4: Diastolic left ventricular dysfunction (LVD) in the two groups


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Moreover, logistic regression analysis showed that after adjustment for age and gender, MS was an independent predictor of both systolic and diastolic LVD [Table 5] and [Table 6].
Table 5: Logistic regression: Predictors of systolic LVD


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Table 6: Logistic regression: predictors of diastolic LVD


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  Discussion Top


In our study, we sought to determine if MS is associated with LVS and/or diastolic dysfunction in patients without symptoms for HF.

In previous studies, we demonstrated that echocardiography can detect preclinical functional or structural myocardial abnormalities in asymptomatic subjects with two or more CVRs and without electrocardiogram abnormalities, [3] and can improve the prognostic impact in comparison to other settings (clinical, ECG). [25] In this survey, asymptomatic patients having diagnosed for MS, were presented with significantly higher prevalence of systolic than patients with only one or two risk factors. More importantly, after adjustment for age and gender, MS proved to be a strong independent predictor of early LV systolic and diastolic dysfunction in this subset of patients.

Our results are consistent with other data available in literature, suggesting that MS leads to an higher risk of ventricular dysfunction involving the myocardium in early stages, before clinical signs of HF. [26] Individual MS markers are inferior to MS in identifying subtle cardiac dysfunction, emphasizing the importance of synergistic effect of these clinical conditions in identifying organ damage. Particularly, among MS criteria, the coexistence of MS and type 2 diabetes exhibits the highest risk for biventricular dysfunction, requiring more aggressive therapeutic strategies to prevent HF. [14]

Furthermore, the number of coexisting characteristics of metabolic syndrome (arterial hypertension, central obesity, hyperglycemia and hypertriglyceridemia) can strongly influence not only the presence, but also the degree of diastolic dysfunction. [27]

It has also been demonstrated that the impact of MS on LV remodeling and diastolic LVD is significantly influenced by gender, since the effects of MS on preclinical LVD were found to be more pronounced in women. [28] However, these data were not confirmed in our study, in which no statistically significant differences were found between sex categories.

In a community-based sample of middle-aged men, metabolic syndrome proved to be a significant predictor of HF, independent of established risk factors for HF, during two decades of follow up. [29] Moreover, data from a large trial on 9306 participants with impaired glucose tolerance and at least one or more CVR, reveal that traditional risk factors and novel indices of central adiposity and increased urinary albumin-creatinine are good predictors of incident hospitalization for HF. [30] This implies that MS provides important risk information beyond that of established risk factors for HF. However, the exact mechanisms are still not clear. Previous data supported the role of insulin resistance, as an important risk factor for the development of hypertension, atherosclerotic heart disease, left ventricular hypertrophy and HF, reflecting that a disturbance of glucose metabolism may potentially worsen metabolic efficiency of both skeletal muscle and cardiac muscle. [30],[31] Some authors proposed that insulin resistance might be promoted by a sympathetic nervous system over activity, characterizing chronic HF and that this neurohormonal disregulation could be potentiated by obesity and MS. [32] Recently, it has been pointed out that superobesity is associated with insulin resistance, with a worse impact on cardiac remodeling and LV diastolic function than morbid obesity. [33]

Consistently with an early myocardial damage, metabolic syndrome was recently found to be associated with decreased mechanical properties of the myocardium, particularly of sub-endocardial fibers, as demonstrated by an impairment of longitudinal myocardial diastolic and systolic functions, but preserved circumferential functions and twist mechanics. [34]

However, our study is the first large national multicenter study providing a real prevalence of asymptomatic LVD in a population with CVR and no symptoms for HF.

Limitations

Limitation of this study is the selection of a sample of patients not representative of entire population, but a selected population with more prone to CVR. Another limitation is that we used BMI rather than waist circumference to define metabolic syndrome. However, this parameter has been accepted by other major studies, in which a close correlation was found between BMI and waist circumference. Moreover, being a national multicenter study, involving more than 75 centers, our protocol did not include tissue Doppler imaging (TDI) or 2-dimensional (2D) strain for longitudinal function and myocardial deformation evaluations, as they are not easily available in all echolabs within the territory. These data might have revealed an early left ventricular dysfunction also in patients with normal EF, unmasking the earliest stages of systolic LVD.


  Conclusion Top


Our data show that in a large sample of asymptomatic patients, the presence of MS is an independent predictive risk factor for asymptomatic systolic and diastolic LVD.

Echocardiographic examination is a useful tool to detect left ventricular alterations in high risk patients, and may help to identify subset of patients prone to develop overt HF. [3],[25] The presence of these alterations may help to introduce lifestyle changes aimed to reducing single risk factors, or lead to establish a prompt pharmacological treatment to prevent future cardiovascular events and/or the progression to symptomatic congestive HF.

Considering the epidemiologic implication of the disease, patients who are at risk for MS, should be screened aggressively for cardio-vascular parameters with the aim of reducing morbidity and mortality, improving quality of life, and also reducing the financial burden.


  Appendix a Daves Investigators Top


M.G. Cherchi (Cardiology, Hospital of Alghero); S. Arcidiacono, G. Chiaranda` (Cardiology, Hospital 'Muscatello', Augusta, SR); A. Scarcia (Cardiology, 'F. Miulli' Hospital, Bari); G. Franchini, M. Ruggiero (Cardiology, 'S. Paolo' Hospital, Bari); M. Sorino, I. De Luca (Cardiology, General Hospital, Bari); N. D'Amato, C. D'Agostino (Cardiology, 'Di Venere' Hospital, Bari); G. Granata, G. Gullace (Cardiology, Hospital of Bellano, LC); G. Ciampa, M. Scherillo (Cardiology, 'Gaetano Rummo' Hospital, Benevento); A.M. Valsecchi, A. Gavazzi (Cardiology, Associated Hospitals, Bergamo); B. Passaretti, E. Perlasca (Cardiology, Clinic 'Gavazzeni', Bergamo); M. Marcolongo, B. Tomassini ('Infermi' Hospital, Biella); G. Labanti, G. Pinelli (Cardiology, Bellaria Hospital, Bologna); L. Latina, W. Pitascheider (Cardiology, General Hospital, Bolzano); E. Chiari, L. Dei Cas (Cardiology, Civili Hospital, Brescia); L. Cossu (Cardiology, Hospital 'Businco', Cagliari); G. Piovesana (Cardiology, Hospital of Camposanpiero, PD); M. Raineri (Cardiology, 'Barone Lombardo' Hospital, Canicattύ`, AG); I. Monte (Cardiology, University of Catania); S. Felis, C. Tamburino (Cardiology, 'Ferrarotto' Hospital, Catania); G. Carnemolla, D. Vanaria (Cardiology,'Ascoli Tomaselli' Hospital, Catania); G. Centamore, G. Lombardo (Cardiology, 'Cannizzaro' Hospital, Catania); F. Gentile (Cardiology, 'Bassini' Hospital, Cinisello Balsamo, MI); M.T. Santis, S. Mandorla (Cardiology, Hospital of Citta` di Castello, PG); G. Corrado, M. Santarone (Cardiology, 'Valduce' Hospital, Como); F. Margaria, L. Lo Sardo ('S. Croce' Hospital, Cuneo); F. Jacopi, R. Casanova (Cardiology, Hospital of Faenza, RA); A. Zuppiroli (Cardiology, 'S.M. Annunziata' Hospital, Firenze); G. Giorgi, P. Verallo (Cardiology, 'S. Sebastiano Martire' Hospital, Frascati, RM); V. Paniccia, G. Faticanti ('Umberto I' Hospital, Frosinone); P. Cassottana, S. Chierchia (Cardiology, 'S. Martino' Hospital, Genova); A. Cresti, S. Severi (Cardiology, 'Della Misericordia'Hospital, Grosseto); S. Fratini (Cardiology, University of L'Aquila); C.A. Greco, F. Magliari (Cardiology, 'Vito Fazzi' Hospital, Lecce); R. Zanini, (Cardiology, 'Carlo Poma' Hospital, Mantova); G. Rubino (Cardiology, Hospital of Marsala, TP); S. Oliva, F. Arrigo (Cardiology, University of Messina); S. Coglitore (Clinical Department of Internal Medicine, University of Messina); A. Mantero, C. Fiorentini (Cardiology, 'San Paolo' Hospital, Milano); P.Piotti, C. Materazzo (National Institute for the Study and Treatment of Cancers, Milano); A. Moreo, F. Mauri (Cardiology, 'Niguarda Ca' Granda' Hospital, Milano); R. Orsi, I. Parrini ('S. Croce Hospital', Moncalieri, TO); T. Monegra, G. Cattarini (Cardiology, Hospital of Monfalcone, VE); D. Iarussi, R. Calabro` (Cardiology, Second University of Napoli); M. De Maio (Cardiology, 'S. Giovanni Bosco' Hospital, Napoli); G. Ferito (Cardiology, Ascalesi Hospital, Napoli); E. Liguori, C. Astarita (Cardiology, Hospital of Sorrento, NA); P. Caso, N. Minnini (Cardiology, 'Monadi' Hospital, Napoli); L. Badano (Cardiology, University of Padova); G. Pumilia, S. Di Rosa (Internal Medicine, 'Villa Sofia Whitaker' Hospital, Palermo); M.C. Sardo ('Torina' Clinic, Palermo); K. Savino, G. Ambrosio (Cardiology, University of Perugia); E. Mariotti ('S. Salvatore' Hospital, Pesaro); A. Falcone, A. Bobili (Cardiology, Hospital of Pescara), V. Di Bello, A. Balbarini (Cardiac-Thoracic Department, University of Pisa); G. Tartarini (Cardiology, Hospital of Pontedera, PI); M. Fasano, G. Argento (Cardiology, 'S. Carlo' Hospital, Potenza); F. Benedetto, F. Tassone (Cardiology, 'E. Morelli' Hospital, Reggio Calabria); M. De Cristofaro, R. Ascoli (Cardiology, 'S. Giovanni di Dio' Hospital, Salerno); D. Pavan (Cardiology, 'S. Maria dei Battuti' Hospital, San Vito al Tagliamento, PN), A. Posteraro, G. Gambelli (Cardiology, 'Policlinico Luigi Di Liegro', Roma); A. Auriti, M. Santini ('S. Filippo Neri' Hospital, Roma); P.G. Pino (Cardiology I, 'San Camillo Forlanini' Hospital, Roma), S. Sciomer, F. Fedele (Cardiovascular and Respiratories Sciences Departiment, 'La Sapienza'University, Roma); G. Limongelli, A. Galati (Cardiology, 'Villa Betania' Hospital, Roma), M.T. Foddanu (Cardiology, Hospital of Sassari); G. Montanari (Cardiology, Hospital of Senigallia, AN); M. Iannopollo (Cardiology, Hospital of Siderno, RC); A. Marotta, G. Bellieni (Cardiology, Hospital of Soveria Mannelli, CZ); C. Napoletano (Cardiology, 'G. Mazzini' Hospital, Teramo); B. Martini, C. Sperotto (Cardiology, Hospital of Thiene, VI); A. Galati, F. De Nuccio (Cardiology,'Cardinale Panico' Hospital, Tricase, LE); M. Massimo (Cardiology, 'Gradenigo' Hospital, Torino); P. Aragona, L. Donnangelo (Cardiology, 'G. Chidichimo' Hospital, Trebisacce, CS); C. Pandullo, S. Scardi (Cardiovascular Center, Health Services 1, Trieste).

 
  References Top

1.Hunt AH, Baker DW, Chin MH, Cinquegrani MP, Feldmanmd AM, Francis GS, et al. ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). Circulation 2001;104:2996-3007.  Back to cited text no. 1
    
2.Carerj S, La Carrubba S, Salustri A, Penco M, Antonini Canterin F, Zito C, et al. Asymptomatic systolic and diastolic dysfunction in patients with risk factors referred for echocardiography. The DAVES study by the Italian Society of Cardiovascular Echography. J Cardiovasc Echogr 2012;22:29-36.  Back to cited text no. 2
    
3.Carerj S, La Carrubba S, Antonini-Canterin F, Di Salvo G, Erlicher A, Liguori E, et al. Research Group of the Italian Society of Cardiovascular Echography. The incremental prognostic value of echocardiography in asymptomatic stage a heart failure. J Am Soc Echocardiogr 2010;23:1025-34.  Back to cited text no. 3
    
4.Aronow WS, Ahn C, Kronzon I. Effect of beta blockers alone, of angiotensin-converting enzyme inhibitors alone, and of beta blockers plus angiotensin-converting enzyme inhibitors on new coronary events and on congestive heart failure in older persons with healed myocardial infarcts and asymptomatic left ventricular systolic dysfunction. Am J Cardiol 2001;88:1298-300.  Back to cited text no. 4
    
5.Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced ejection fractions. The SOLVD Investigators. N Engl J Med 1992;327:685-91.  Back to cited text no. 5
    
6.Dargie HJ. Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: The CAPRICORN randomised trial. Lancet 2001;357:1385-90.  Back to cited text no. 6
    
7.Redfield MM, Jacobsen SJ, Burnett JC Jr, Mahoney DW, Bailey KR, Rodeheffer RJ. Burden of systolic and diastolic ventricular dysfunction in the community: Appreciating the scope of the heart failure epidemic. JAMA 2003;289:194-202.  Back to cited text no. 7
    
8.Wang TJ, Levy D, Benjamin EJ, Vasan RS. The epidemiology of "asymptomatic" left ventricular systolic dysfunction: Implications for screening. Ann Intern Med 2003;138:907-16.  Back to cited text no. 8
    
9.Reaven GM. Banting lecture 1988: Role of insulin resistance in human disease. Diabetes 1988;37:1595-607.  Back to cited text no. 9
    
10.Third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III). Final report. Circulation 2002;106:3143-421.  Back to cited text no. 10
    
11.Butler J, Rodondi N, Zhu Y, Figaro K, Fazio S, Vaughan DE, et al. Health ABC Study. Metabolic syndrome and the risk of cardiovascular disease in older adults. J Am Coll Cardiol 2006;47:1595-602.  Back to cited text no. 11
    
12.de Simone G, Devereux RB, Chinali M, Best LG, Lee ET, Galloway JM, et al. Strong Heart Study Investigators. Prognostic impact of metabolic syndrome by different definitions in a population with high prevalence of obesity and diabetes: The Strong Heart Study. Diabetes Care 2007;30:1851-6.  Back to cited text no. 12
    
13.Li C, Ford ES, McGuire LC, Mokdad AH. Association of metabolic syndrome and insulin resistance with congestive heart failure: Findings from the Third National Health and Nutrition Examination Survey. J Epidemiol Community Health 2007;61:67-73.  Back to cited text no. 13
    
14.Paneni F, Gregori M, Tocci G, Palano F, Ciavarella GM, Pignatelli G, et al. Do diabetes, metabolic syndrome or their association equally affect biventricular function? A tissue Doppler study. Hypertens Res 2013;36:36-42.  Back to cited text no. 14
    
15.Quinones MA, Douglas PS, Foster E, Gorcsan J, Lewis JF, Pearlman AS, et al. ACC/AHA clinical competence statement on echocardiography: A report of the American College of Cardiology/American Heart Association/American College of Physicians - American Society of Internal Medicine Task Force on Clinical Competence (Committee on Echocardiography). J Am Coll Cardiol 2003;41:687-708.  Back to cited text no. 15
    
16.Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al. American Heart Association; National Heart, Lung, and Blood Institute. Diagnosis and management of the metabolic syndrome: An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation 2005;112:2735-52.  Back to cited text no. 16
    
17.Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A, Bohm M, et al. ESH/ESC Guidelines for the management of arterial hypertension The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J 2013;34:2159-219.  Back to cited text no. 17
    
18.Reiner Z, Catapano AL, De Backer G, Graham I, Taskinen MR, Wiklund O. ESC/EAS Guidelines for the management of dyslipidaemias. The Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS). Eur Heart J 2011;32:1769-818.  Back to cited text no. 18
    
19.The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 1997;20:1183-97.  Back to cited text no. 19
    
20.Sattar N, Gaw A, Scherbakova O, Ford I, O'Reilly DS, Haffner S, et al. Metabolic syndrome with and without C-reactive protein as a predictor of coronary heart disease and diabetes in the West of Scotland Coronary Prevention Study. Circulation 2003;2:414-9.  Back to cited text no. 20
    
21.Hamaguchi M, Kojima T, Takeda N, Nakagawa T, Taniguchi H, Fujii K, et al. The metabolic syndrome as a predictor of nonalcoholic fatty liver disease. Ann Intern Med 2005;143:722-8.  Back to cited text no. 21
    
22.Sattar N, Gaw A, Scherbakova O, Ford I, O'Reilly DS, Haffner SM, et al. Metabolic syndrome with and without C-reactive protein as a predictor of coronary heart disease and diabetes in the West of Scotland Coronary Prevention Study. Circulation 2003;108:414-9.  Back to cited text no. 22
    
23.Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989;2:358-67.  Back to cited text no. 23
    
24.Khouri SJ, Maly GT, Suh DD, Walsh TE. A practical approach to the echocardiographic evaluation of diastolic function. J Am Soc Echocardiogr 2004;17:290-7.  Back to cited text no. 24
    
25.Bello VD, Carrubba SL, Antonini-Canterin F, Salvo GD, Caso P, Canna GL, et al. On behalf of the Research Group of the Italian Society of Cardiovascular Echography (SIEC), Milan, Italy. Role of electrocardiography and echocardiography in prevention and predicting outcome of subjects at increased risk of heart failure. Eur J Prev Cardiol 2013.  Back to cited text no. 25
    
26.Hermida N, Markl A, Hamelet J, Van Assche T, Vandersper A, Herijers P, et al. HMGCoA reductase inhibition reverses myocardial fibrosis and diastolic dysfunction through AMP-activated protein kinase activation in a mouse model of metabolic syndrome. Cardiovasc Res 2013.  Back to cited text no. 26
    
27.Penjaskoviæ D, Sakac D, Dejanoviæ J, Zec R, Zec Petkovic N, Stojsiæ Milosavljeviæ A. Left ventricular diastolic dysfunction in patients with metabolic syndrome. Med Pregl 2012;65:18-22.  Back to cited text no. 27
    
28.Nicolini E, Martegani G, Maresca AM, Marchesi C, Dentali F, Lazzarini A, et al. Left ventricular remodeling in patients with metabolic syndrome: Influence of gender Nutr Metab Cardiovasc Dis 2013;23:771-5.  Back to cited text no. 28
    
29.Ingelsson E, Arnlov J, Lind L, Sundstrom J. Metabolic syndrome and risk for heart failure in middle-aged men. Heart 2006;92:1409-13.  Back to cited text no. 29
    
30.Giles TD, Sander GE. Diabetes mellitus and heart failure: Basic mechanisms, clinical features, and therapeutic considerations. Cardiol Clin 2004;22:553-68.  Back to cited text no. 30
    
31.Coats AJ, Anker SD. Insulin resistance in chronic heart failure. J Cardiovasc Pharmacol 2000;35:S9-14.  Back to cited text no. 31
    
32.Grassi G, Seravalle G, Quarti-Trevano F, Scopelliti F, Dell'Oro R, Bolla G, et al. Excessive sympathetic activation in heart failure with obesity and metabolic syndrome: Characteristics and mechanisms. Hypertension 2007;49:535-41.  Back to cited text no. 32
    
33.Antonini-Canterin F, Mateescu AD, Vriz O, La Carrubba S, Di Bello V, Carerj S, et al. Cardiac structure and function and insulin resistance in morbidly obese patients: Does superobesity play an additional role? Cardiology 2013;127:144-51.  Back to cited text no. 33
    
34.Crendal E, Walther G, Vinet A, Dutheil F, Naughton G, Lesourd B, et al. Myocardial deformation and twist mechanics in adults with metabolic syndrome: Impact of cumulative metabolic burden. Obesity (Silver Spring) 2013;21:E679-86.  Back to cited text no. 34
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]



 

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