scholarly journals Objective Evidence of Pulsus Alternans by Echocardiography in Acute Severe Heart Failure

2020 ◽  
Vol 16 (2) ◽  
pp. 92-98
Author(s):  
Nilufar Fatema ◽  
Rayhan Masum Mandal ◽  
Jahanara Arzu ◽  
SM Ahsan Habib ◽  
Khurshed Ahmad ◽  
...  

Acute coronary syndrome may leads to heart failure. Severity of heart failure is identified by NYHA classification clinically. Color Doppler echocardiography is the key investigation to identify the acute systolic heart failure. For the quantification of systolic heart failure diagnosis, Ejection fraction (EF) can be measured by Simpson method. EF > 30% is defined as severe systolic heart failure. Pulsus alternans is found in severe heart failure patients. Pulsus alternans is a poor prognostic sign of severe heart failure patients in acute MI setting. This cross sectional observation study was aimed to identify the objective evidence of Pulsus alternance noninvasively by Echocardiography. Color Doppler echocardiography was done 100 acute coronary syndrome with heart failure NYHA III and IV patients in department of Cardiology, BSMMU, from July 2018 to June 2019. Age 18 to 70 yrs, male is 79 and female is 21. Pulsus alternans was found in 32 patients, 39 had low volume and 29 had normal volume pulse. 50% patients had ST depression and T inversion and diagnosed as case of Unstable Agina or Non STEMI, 44 had STEMI and 7 had developed new onset of LBBB. 87 Patients who have EF < 30 % was marked as Severe LV systolic dysfunction. Among them, 3 had mild, 14 had moderate and rest 70 had severe Mitral regurgitation. 38 (43.67%) patients had Doppler alternans in severe LV systolic dysfunction group. P value for Doppler alternans is 0.039 which is significant. Doppler alternans by Echocardiography in Severe LV systolic dysfunction patients showed 49% sensitivity and 78% specificity. 38 patients had Severe RV systolic dysfunction by M- mode echo measurement of TAPSE<10 mm. 22 (57.89%) had Doppler alternans across Tricuspid valve in case of severe RV systolic dysfunction. Sensitivity of Doppler alternans by Doppler Echocardiography in TV severe RV systolic dysfunction is 51% and specificity for it is 82%. University Heart Journal Vol. 16, No. 2, Jul 2020; 92-98

2016 ◽  
Author(s):  
Alexey B. Terentjev ◽  
Scott H. Settlemier ◽  
Douglas P. Perrin ◽  
Pedro J. del Nido ◽  
Igor V. Shturts ◽  
...  

1999 ◽  
Vol 5 (3) ◽  
pp. 79
Author(s):  
John S. Golden ◽  
Catherine Chelimsky-Fallick ◽  
Donna J. Mateski ◽  
Colleen M. Healey ◽  
Sharon R. Josephson ◽  
...  

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Jorge E Massare ◽  
R. Haris Naseem ◽  
Jeff M Berry ◽  
Farhana Rob ◽  
Joseph A Hill

Background: Sudden cardiac death due to ventricular tachyarrhythmia (VT) accounts for a large number of deaths in patients with heart failure. Several cellular events which occur during pathological remodeling of the failing ventricle are implicated in the genesis of VT, including action potential prolongation, dysregulation of intercellular coupling, and fibrosis. Interestingly, transgenic mice over-expressing constitutively active PKD (caPKD) develop severe heart failure without interstitial fibrosis, an otherwise prominent feature of the disease. The goal here was to define the role of interstitial fibrosis in the proarrhythmic phenotype of failing myocardium. Methods and Results: We performed echocardiographic, electrocardiographic, and in vivo electrophysiologic studies in 8 –10 week old caPKD mice (n=12). Similar studies were performed in mice with load-induced heart failure induced by surgical pressure overload (sTAB, n=10), a model of heart failure with prominent interstitial fibrosis. caPKD and sTAB mice showed similar degrees of ventricular dilation (LV systolic dimension caPKD 2.4±0.8 mm vs 3.0±0.9 sTAB, p=0.18) and severe systolic dysfunction (% fractional shortening caPKD 25±11 vs 28±11 sTAB, p=0.62). Yet, caPKD mice showed minimal interstitial fibrosis, comparable to unoperated controls. With the exception of ventricular refractory period, which was higher in caPKD (48±11 msec vs 36±7 TAB and 40±8 WT, p<0.05), other electrocardiographic and electrophysiologic variables were similar among the 3 groups (p=NS), including heart rate, QT duration, and mean VT threshold. As expected, VT (≥3beats) was readily inducible by programmed stimulation in sTAB mice (7/10). By contrast, VT was less inducible in caPKD mice (4/12; p=0.1 vs TAB and <0.05 vs WT), and uninducible in unoperated controls (0/12). VT was polymorphic in both models, but episodes of VT were both slower (VT cycle length caPKD 58±4.0 msec vs 48±1 sTAB, p=0.016) and longer in caPKD mice (caPKD 1.8±0.7 sec vs 0.47±0.3 sTAB, p=0.038). Conclusion: Interstitial fibrosis contributes to the inducibility, maintenance, and rate of VT in heart failure. These findings highlight the importance of anti-remodeling therapies known to target fibrosis in heart disease.


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