scholarly journals Subcellular remodelling may induce cardiac dysfunction in congestive heart failure

2008 ◽  
Vol 81 (3) ◽  
pp. 429-438 ◽  
Author(s):  
N. S. Dhalla ◽  
H. K. Saini-Chohan ◽  
D. Rodriguez-Leyva ◽  
V. Elimban ◽  
M. R. Dent ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Dysfunction

scholarly journals Role of Subcellular Remodeling in Cardiac Dysfunction due to Congestive Heart Failure

2007 ◽  
Vol 16 (2) ◽  
pp. 81-89 ◽  
Author(s):  
Andrea P. Babick ◽  
Naranjan S. Dhalla
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Dysfunction

scholarly journals Comparison of Red Cell Distribution Width (RDW) Value in Congestive Heart Failure (CHF) Patients with Normal Persons

2021 ◽  
Vol 8 (8) ◽  
pp. 27-30
Author(s):  
Marhani Yunita ◽  
Herman Hariman
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Dysfunction ◽  
Red Cell Distribution Width ◽  
Hematological Parameter ◽  
Red Cell ◽  
Cell Distribution ◽  
Distribution Width ◽  
Normal People ◽  
Significant Difference

Congestive Heart Failure (CHF) is a complex clinical symptom that is often characterized by structural abnormalities or cardiac dysfunction that impairs the ability of the left ventricle (LV) to fill or pump blood, especially during physical activity. Red Cell Distribution Width (RDW) is a simple, fast, inexpensive and direct hematological parameter, which reflects the level of anisocytosis in vivo. The association between impaired hematopoiesis and cardiac dysfunction is based on the fact that many different conditions are associated with increased heterogeneity of erythrocyte volume, which can be concurrently present in patients with heart failure, while anisocytosis can also directly contribute to the development and worsening of heart failure. This study aims to provide a comparison of RDW values between CHF patients and normal people. This study uses a case control study design where as many as 20 people with CHF will be compared their RDW values with 20 normal people. From a total of 40 patients, the average RDW value in CHF patients was 17.7±2.4 higher than the average RDW value for normal people was 12.6±0.4 and from the results of statistical analysis using the Independent Student t test obtained p value <0.001. There is a significant difference between the RDW values of CHF patients compared to normal people. Keywords: Congestive Heart Failure, CHF, Red Cell Distribution Width, RDW.

Acute hemodynamic effects of bunazosin in congestive heart failure—Differing responses according to degree of cardiac dysfunction

1993 ◽  
Vol 24 (4) ◽  
pp. 899-904
Author(s):  
Kazuhide Ogino ◽  
Noriyasu Noguchi ◽  
Shuichi Osaki ◽  
Hideyuki Kitamura ◽  
Tatsuhiko Matsumoto ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Dysfunction ◽  
Hemodynamic Effects

Inhibition of NOS II prevents cardiac dysfunction in myocardial infarction and congestive heart failure

2002 ◽  
Vol 283 (1) ◽  
pp. H339-H345 ◽  
Author(s):  
Takayuki Saito ◽  
Fu Hu ◽  
Lara Tayara ◽  
Linda Fahas ◽  
Hani Shennib ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Function ◽  
Infarct Size ◽  
Cardiac Dysfunction ◽  
Cardiomyocyte Hypertrophy ◽  
Lung Water ◽  
Term Administration

Strong expression of the inducible form of nitric oxide synthase (NOS II) has been shown in the myocardium of patients with myocardial infarction (MI). We hypothesized that NOS II plays an important role in the development of MI and subsequent heart failure and that inhibition of NOS II may beneficially alter the course of the disease. Long-term administration (2 mo) of the selective NOS II inhibitor S-methylisothiourea (SMT) to rats with MI significantly improved cardiac function. A significant drop in mortality, lung water content, infarct size, and cardiomyocyte hypertrophy was also associated with the use of SMT. Plasma concentration of nitrite and nitrate was also reduced by SMT. Short-term administration of SMT (first 2 wk only) significantly reduced infarct size; however, it did not improve cardiac dysfunction measured 2 mo after MI. These findings demonstrate that induction of NOS II during MI exerts negative effects on cardiac function and structure. Long-term administration of a selective NOS II inhibitor may prove to be beneficial in the treatment of MI and congestive heart failure.

scholarly journals β-adrenergic blockade attenuates cardiac dysfunction and myofibrillar remodelling in congestive heart failure

2010 ◽  
Vol 15 (3) ◽  
pp. 545-554 ◽  
Author(s):  
Jarmila Machackova ◽  
Santosh K. Sanganalmath ◽  
Vijayan Elimban ◽  
Naranjan S. Dhalla
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Dysfunction ◽  
Adrenergic Blockade

Left Sided Heart Dysfunction in Sickle Cell Disease: Echocardiographic and Genetic Studies.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 78-78 ◽  
Author(s):  
Laura M. De Castro ◽  
Jude C. Jonassaint ◽  
Marilyn J. Telen
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Sickle Cell Disease ◽  
Sudden Death ◽  
Sickle Cell ◽  
Cardiac Dysfunction ◽  
Left Ventricular ◽  
Valve Regurgitation ◽  
Cell Disease ◽  
High Output

Abstract The moderate to severe anemia associated with sickle cell disease (SCD) causes a high output state that can lead to cardiomyopathy, decompensation and left heart failure. While at least one report suggested that chronic high output and volume overload are relatively well tolerated in SCD, other studies have suggested that congestive heart failure and other cardiac abnormalities may occur in more than 50% of adults. The incidence of sudden death is also increased and may be as high as 40% in adults with SCD. Several types of left ventricular (LV) dysfunction are associated with sudden death in other populations, although an association of LV disease and sudden death in SCD has not been studied. For these reasons, and also based on the clinical observation that SCD patients frequently experience transient episodes of clinical congestive heart failure (especially when receiving intravenous fluids during vaso-occlusive episodes), we sought to document the frequency with which left-sided cardiac dysfunction existed in our patient population. We performed a retrospective review of resting echocardiograms to quantitate multiple parameters of cardiac function in patients either homozygous for hemoglobin S or with Sβ0 thalassemia. 116 patients had had at least one echocardiogram performed (55 females, mean age 37, range 13–71; 61 males, mean age 32, range 16–62). 31% of these patients (mean age 41) had left ventricular hypertrophy (LVH), defined as a left ventricular mass index ≥134 and ≥110 g/m2 for men and women, respectively, and 22% (mean age 35) had left ventricular enlargement. Of the 36 patients with LVH, 27 had mild LVH, and 9 had moderate-severe LVH. Presence and severity of LVH were significantly related to mean arterial blood pressure (p=0.004), even though most patients were not hypertensive. Mean arterial pressures were also related to posterior LV wall thickness (p&lt;0.0001), and baseline hemoglobin level was inversely associated with posterior wall thickness (p=0.0001). In addition, 53% had left atrial (LA) enlargement, 9% had mild-moderate aortic valve regurgitation, and 37% had mild-moderate mitral valve regurgitation (MR), with an additional 45% having trivial MR. Of all 116 patients studied, 61% (mean age 41, range 21–66) had pulmonary hypertension (pHTN), as indicated by a reported tricuspid regurgitant jet velocity of ≥2.5 m/s. In the patient group with LV enlargement, 75% of patients had pHTN, while of patients with LVH, 77% had pHTN. LA enlargement was also significantly more common in patients who had pHTN (p=0.002). While only 10% of patients had an ejection fraction below 55%, 37% (mean age 37) had fractional shortening (FS) less than 0.30. This suggests the presence of limited cardiac reserve in relatively young patients, as decreased FS is generally a finding that precedes a decrease in cardiac output. We have also begun to identify genetic polymorphisms that are associated with cardiac dysfunction. Two polymorphisms in the β2 adrenergic receptor gene were associated with either LA enlargement (rs1042713, p=0.02) and/or presence of LVH or LV enlargement (rs1042713, p=0.001; rs1042717, p=0.04). Polymorphisms of the adenylate cyclase 6 gene were also associated with LA enlargement (hcv1244841, p=0.02) and LV function as measured by FS (rs370070, p=0.01). In summary, these data demonstrate the significant prevalence of left-sided cardiac dysfunction in SCD. We hypothesize that these abnormalities contribute to progressive physical limitations, as well as sudden death. The pathophysiology of high output heart failure in this setting therefore merits considerable further study.

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