scholarly journals Therapy potential for the correction of cardiovascular disturbances in diabetes mellitus

2012 ◽  
Vol 11 (4) ◽  
pp. 59-64
Author(s):  
I. P. Tatarchenko ◽  
N. V. Pozdnyakova ◽  
A. G. Mordovina ◽  
O. I. Morozova ◽  
E. V. Rubleva

Aim. To study the dynamics of left ventricular (LV) structure and function, as well as vasomotor activity of arterial endothelium, in patients with Type 2 diabetes mellitus (DM-2) and diastolic heart failure (DHF) who are treated with an angiotensin II receptor antagonist olmesartan. Material and methods. The study included 56 patients (26 men and 30 women; mean age 58,2±5,3 years) with NYHA Functional Class I-II chronic heart failure (CHF), diastolic LV dysfunction (abnormal relaxation), and LV ejection fraction (EF) >50%. Other inclusion criteria were DM-2 duration <15 years and per os glucoselowering treatment. Results. The major pathogenetic mechanisms of LV diastolic dysfunction and endothelial dysfunction in DM-2 are linked to the development of central sympathetic hyperactivation and activation of the tissue reninangiotensin system. Conclusion. After 30 weeks of olmesartan therapy, LV structure and geometry, LV diastolic function, and vasomotor activity of arterial endothelium had improved, which was expected to reduce the risk of myocardial ischemia.

2013 ◽  
Vol 58 (6) ◽  
pp. 8-12
Author(s):  
I. P. Tatarchenko ◽  
N. V. Pozdnyakova ◽  
A. G. Mordovina

Cardiovascular disorders are the main cause of high disability and mortality rates among the patients with diabetes mellitus. The objective of the present work was to estimate the clinical and hemodynamic characteristics during the treatment of arterial hypertension with the use of olmesartan (hypertension/angiotensin II receptor antagonist, ARA) in the patients with type 2 diabetes mellitus suffering diastolic heart failure. The study included 56 patients (26 men and 30 women) of the mean age 58.2±5.3 years. They were given a course of olmesartan (cardosal) therapy 40 weeks in duration. This treatment was shown to result in positive dynamics of structural and geometric characteristics of the left ventricle and its diastolic function in conjunction with the improvement of the vasomotor function of arterial endothelium.


2013 ◽  
Vol 5 (1) ◽  
Author(s):  
Starry H Rampengan

Abstract: Diastolic heart failure (HF) is also referred to as heart failure with normal left ventricular systolic function (normal ejection fraction). The difference between the systolic and diastolic HFs is based on their pathophysiology. In the diastolic HFs, the left ventricular function is normal or slightly impaired. The typical manifestations have an increased filling pressure caused by impaired relaxation and compliance of the left ventricle. The management of diastolic HFs includes antihypertensive treatment, maintenance of the sinus rhythm, prevention of tachycardia, reduction of venous pressure, prevention of myocardial ischemia, and prevention of diabetes mellitus. The aim of the diastolic HFs is: to reduce the progression, to relieve its symptoms, to eliminate exacerbations, and to reduce the mortality. The predisposing factors for the diastolic dysfunction include elderly age, female sex, obesity, coronary artery disease, hypertension, and diabetes mellitus. The European Society of Cardiology specifies therapy in diastolic HFs based on: angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, non-dihydropyridine calcium channel blockers, and diuretics. Keywords: diastolic heart failure, management.     Abstrak: Gagal jantung diastolik disebut juga sebagai gagal jantung dengan fungsi sistolik ventrikel kiri yang normal (fraksi ejeksi normal). Perbedaan antara gagal jantung sistolik dan diastolik terletak pada patofisiologinya. Pada gagal jantung diastolik fungsi ventrikel kiri normal atau sedikit menurun. Manifestasi yang timbul disebabkan oleh peningkatan tekanan pengisian yang diakibatkan oleh gangguan relaksasi dan komplains ventrikel kiri. Manajemen gagal jantung diastolik meliputi terapi antihipertensi, pemeliharaan irama sinus, pencegahan takikardi, pengurangan tekanan vena, pencegahan iskemik miokard dan pencegahan diabetes melitus. Tujuan terapi gagal jantung diastolik yaitu mengurangi progresivitas, menghilangkan gejala, mencegah eksaserbasi dan menurunkan angka mortalitas. Faktor predisposisi disfungsi diastolik meliputi usia lanjut, jenis kelamin wanita, obesitas, penyakit jantung koroner, hipertensi, dan diabetes melitus. The European Society of Cardiology mengeluarkan beberapa macam penatalaksanaan gagal jantung diastolik berdasarkan: ACE-inhibitors, angiotensin receptor blocker, beta blocker, non dihydropiridine calcium channel blocker, dan diuretik. Kata kunci: gagal jantung diastolik, penatalaksanaan.


2010 ◽  
Vol 6 (3) ◽  
pp. 13 ◽  
Author(s):  
Bogdan A Popescu ◽  
Carmen C Beladan ◽  
Carmen Ginghină ◽  
◽  
◽  
...  

A normal ejection fraction (EF) is present in >50% of patients with clinical features of heart failure (HF). This entity has been referred to as HF with normal EF (HFNEF), or diastolic HF. The underlying pathophysiology of HFNEF is still under debate and this is reflected in the unsatisfactory results of pharmacological treatment and in the high mortality and morbidity rates, which are similar to those for systolic HF. By providing evidence of left ventricular (LV) diastolic dysfunction in patients with clinical features of HF and normal LVEF, echocardiography, the most practical and widely available diagnostic modality, can offer two of the three current diagnostic criteria for HFNEF. Moreover, abnormalities in LV myocardial deformation and torsional dynamics at rest and during exercise were recently demonstrated in HFNEF patients by echocardiography. Newer echocardiographic parameters may improve the understanding of this complex entity, but further studies are needed before using them in clinical practice for the diagnostic and therapeutic approach of patients with HFNEF. This article discusses the current echocardiographic approach to the diagnosis of diastolic HF, as well as the potential role of newer echo indices and modalities.


2015 ◽  
pp. 50-8
Author(s):  
Starry H. Rampengan

The diastolic heart failure also referred to as heart failure with preserved left ventricular systolic function (preserved ejection fraction). The difference between systolic and diastolic HFs is a pathophysiological one and isolated forms of left ventricular dysfunction are rarely observed. In diastolic HF left ventricular systolic function is normal or only slightly impaired, and the typical manifestations of HF result from increased filling pressure caused by impaired relaxation and compliance of the left ventricle. The management should include antihypertensive treatment, maintenanceof the sinus rhythm, prevention of tachycardia, venous pressure reduction, prevention of myocardial ischemia and prevention of diabetes mellitus. Treatment of diastolic HF is aimed to stop the progression of the disease, relieve its symptoms, eliminate exacerbations and reduce the mortality. The predisposing factors for diastolic dysfunction include elderly age, female sex, obesity, coronary artery disease, hypertension and diabetes mellitus. The European Society of Cardiology specifies the type of therapy in diastolic HF based on: angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, non dihydropyridine calcium channel blockers, diuretics.


Heart ◽  
2019 ◽  
Vol 106 (8) ◽  
pp. 562-568 ◽  
Author(s):  
Katherine C Wood ◽  
Mark T Gladwin ◽  
Adam C Straub

Sickle cell disease (SCD) is caused by a single point mutation in the gene that codes for beta globin synthesis, causing haemoglobin polymerisation, red blood cell stiffening and haemolysis under low oxygen and pH conditions. Downstream effects include widespread vasculopathy due to recurring vaso-occlusive events and haemolytic anaemia, affecting all organ systems. Cardiopulmonary complications are the leading cause of death in patients with SCD, primarily resulting from diastolic heart failure (HF) and/or pulmonary hypertension (PH). HF in SCD often features biventricular cardiac hypertrophy and left ventricular (LV) diastolic dysfunction. Among HF cases in the general population, approximately half occur with preserved ejection fraction (HFpEF). The insidious evolution of HFpEF differs from the relatively acute evolution of HF with reduced ejection fraction. The PH of SCD has diverse origins, which can be pulmonary arterial (precapillary), pulmonary venous (postcapillary) or pulmonary thromboembolic. It is also appreciated that patients with SCD can develop both precapillary and postcapillary PH, with elevations in LV diastolic pressures, as well as elevations in transpulmonary pressure gradient and pulmonary vascular resistance. Regardless of the cause of PH in SCD, its presence significantly reduces functional capacity and increases mortality. PH that occurs in the presence of HFpEF is usually of postcapillary origin. This review aims to assemble what has been learnt from clinical and animal studies about the manifestation of PH-HFpEF in SCD, specifically the contributions of LV diastolic dysfunction and myocardial fibrosis, in an attempt to gain an understanding of its evolution.


2012 ◽  
Vol 9 (1) ◽  
pp. 90-95 ◽  
Author(s):  
Otto A Smiseth ◽  
Anders Opdahl ◽  
Espen Boe ◽  
Helge Skulstad

Heart failure with preserved left ventricular ejection fraction (HF-PEF), sometimes named diastolic heart failure, is a common condition most frequently seen in the elderly and is associated with arterial hypertension and left ventricular (LV) hypertrophy. Symptoms are attributed to a stiff left ventricle with compensatory elevation of filling pressure and reduced ability to increase stroke volume by the Frank-Starling mechanism. LV interaction with stiff arteries aggravates these problems. Prognosis is almost as severe as for heart failure with reduced ejection fraction (HF-REF), in part reflecting co-morbidities. Before the diagnosis of HF-PEF is made, non-cardiac etiologies must be excluded. Due to the non-specific nature of heart failure symptoms, it is essential to search for objective evidence of diastolic dysfunction which, in the absence of invasive data, is done by echocardiography and demonstration of signs of elevated LV filling pressure, impaired LV relaxation, or increased LV diastolic stiffness. Antihypertensive treatment can effectively prevent HF-PEF. Treatment of HF-PEF is symptomatic, with similar drugs as in HF-REF.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 256-OR ◽  
Author(s):  
JAGDEEP S.S. SINGH ◽  
IFY MORDI ◽  
MOHAPRADEEP MOHAN ◽  
STEPHEN J. GANDY ◽  
EWAN PEARSON ◽  
...  

2005 ◽  
Vol 46 (3) ◽  
pp. 262-268 ◽  
Author(s):  
Pierre V Ennezat ◽  
Caroline A Ennezat ◽  
Pugazhendhi Vijayaraman ◽  
Justine Lachmann ◽  
Philippe Asseman ◽  
...  

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Mohammed Siddiqui ◽  
Salpy V Pamboukian ◽  
Jose A Tallaj ◽  
Michael Falola ◽  
Sula Mazimba

Background: Reducing 30 day readmission rates for patients with heart failure (HF) has been a recent focus of lowering health care expenditures. Hemodynamic profiles (HP) have been associated with clinical outcomes in chronic systolic HF. The relationship of HP to outcomes in acute decompensated diastolic HF (DHF) has not been defined. Methods: This case-control study of 1892 DHF patients discharged alive from an academic hospital between 2002-2012 with left ventricular function greater or equal to 45% were categorized into 4 groups: Profile A, no evidence of congestion and hypoperfusion (dry-warm); Profile B, congestion with adequate perfusion (wet-warm); Profile C, congestion with hypoperfusion (wet-cold); and Profile L, hypoperfusion without congestion (dry-cold). All cause readmissions at 30 days and 1 year and mortality at 30 days and 1 year were examined. Statistical analysis using multivariable Cox Proportional hazard model was performed adjusting for demographic, clinical, care and hospital characteristics. Results: Of the 1892 patients, 1196 (63%) were females; mean age was 68 (±14) years. There were 724(38%), 1000 (53%), 88(5%) and 80 (4%) patients in the hemodynamic profiles A, B, C and L respectively. Profiles B and C were associated with an increased risk for 30-day all-cause HF readmission compared to profiles A and L: Hazard ratio (HR) [1.38 (95% C.I 1.17-1.61)], [1.39 (95% C.I 1.18-1.62)] for B and C profiles respectively. Profiles C and L were associated with increased mortality at 1 year: HR [1.46 (95% CI 1.06-1.89)] and [1.31 (95% CI 1.01-1.64)] for A and L profiles respectively (Table). Conclusions: Clinical assessment of HP can help identify DHF patients at increased risk of readmission and mortality, similar to systolic heart failure patients.


2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Marie Schroeder ◽  
Angus Z Lau ◽  
Albert P Chen ◽  
Jennifer Barry ◽  
Damian J Tyler ◽  
...  

Disordered metabolic substrate utilisation has been implicated in the pathogenesis of heart failure (HF). Hyperpolarised (HYP) 13C magnetic resonance, a technique in which the fate of 13C-labelled metabolites can be followed using MR imaging or spectroscopy, has enabled non-invasive assessment of metabolism. The aim of this study was to monitor carbohydrate metabolism alongside cardiac structure, function, and energetics, throughout HF progression. HF was induced in pigs (n=5) by right ventricular pacing at 188 bpm for 5 weeks. Pigs were examined at weekly time points: cine MRI assessed cardiac structure and function, HYP 13C2-pyruvate was administered intravenously and 13C MRS was used to assess 13C-glutamate production via Krebs cycle, 31P MRS assessed myocardial energetics, and HYP 13C1-pyruvate was administered to enable MRI of H13CO3- production from pyruvate dehydrogenase (PDH). At baseline, pigs had a normal left ventricular (LV) cardiac index (CI) and end diastolic volume (EDVi). The PCr/ATP was 2.3 ± 0.2. The 13C-glutamate/13C2-pyruvate was 4.3 ± 0.9%, and the H13CO3-/13C1-pyruvate ratio was 1.6 ± 0.2%. After 1–2 weeks of pacing, CI decreased to 3.3 ± 0.5 l/min/m2, PCr/ATP decreased to 1.7 ± 0.1, and 13C-glutamate/13C2-pyruvate decreased to 2.1 ± 0.6%. With the onset of HF, EDVi increased to 140.3 ± 14.1 ml/m2 and H13CO3-/13C1-pyruvate decreased to 0.5 ± 0.2%. In conclusion, we observed an early defect in Krebs' cycle that occurred alongside impaired cardiac energetics and function. Carbohydrate oxidation via PDH was maintained until the onset of HF. These results encourage use of metabolic therapies to delay/prevent the onset of heart failure in patients.


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