scholarly journals Response to Letter Regarding Article, “The Effect of Selective Heart Rate Slowing in Heart Failure With Preserved Ejection Fraction”

Circulation ◽  
2016 ◽  
Vol 133 (16) ◽  
Author(s):  
Nikhil Pal ◽  
Nadiya Sivaswamy ◽  
Masliza Mahmod ◽  
Arash Yavari ◽  
Amelia Rudd ◽  
...  
Circulation ◽  
2015 ◽  
Vol 132 (18) ◽  
pp. 1719-1725 ◽  
Author(s):  
Nikhil Pal ◽  
Nadiya Sivaswamy ◽  
Masliza Mahmod ◽  
Arash Yavari ◽  
Amelia Rudd ◽  
...  

2020 ◽  
Vol 9 (17) ◽  
Author(s):  
Daniel N. Silverman ◽  
Mehdi Rambod ◽  
Daniel L. Lustgarten ◽  
Robert Lobel ◽  
Martin M. LeWinter ◽  
...  

Background Increases in heart rate are thought to result in incomplete left ventricular (LV) relaxation and elevated filling pressures in patients with heart failure with preserved ejection fraction (HFpEF). Experimental studies in isolated human myocardium have suggested that incomplete relaxation is a result of cellular Ca 2+ overload caused by increased myocardial Na + levels. We tested these heart rate paradigms in patients with HFpEF and referent controls without hypertension. Methods and Results In 22 fully sedated and instrumented patients (12 controls and 10 patients with HFpEF) in sinus rhythm with a preserved ejection fraction (≥50%) we assessed left‐sided filling pressures and volumes in sinus rhythm and with atrial pacing (95 beats per minute and 125 beats per minute) before atrial fibrillation ablation. Coronary sinus blood samples and flow measurements were also obtained. Seven women and 15 men were studied (aged 59±10 years, ejection fraction 61%±4%). Patients with HFpEF had a history of hypertension, dyspnea on exertion, concentric LV remodeling and a dilated left atrium, whereas controls did not. Pacing at 125 beats per minute lowered the mean LV end‐diastolic pressure in both groups (controls −4.3±4.1 mm Hg versus patients with HFpEF −8.5±6.0 mm Hg, P =0.08). Pacing also reduced LV end‐diastolic volumes. The volume loss was about twice as much in the HFpEF group (controls −15%±14% versus patients with HFpEF −32%±11%, P =0.009). Coronary venous [Ca 2+ ] increased after pacing at 125 beats per minute in patients with HFpEF but not in controls. [Na + ] did not change. Conclusions Higher resting heart rates are associated with lower filling pressures in patients with and without HFpEF. Incomplete relaxation and LV filling at high heart rates lead to a reduction in LV volumes that is more pronounced in patients with HFpEF and may be associated with myocardial Ca 2+ retention.


2017 ◽  
Vol 19 (11) ◽  
pp. 1504-1506 ◽  
Author(s):  
Andreas P. Kalogeropoulos ◽  
Javed Butler

2018 ◽  
Vol 131 (12) ◽  
pp. 1473-1481 ◽  
Author(s):  
Phillip H. Lam ◽  
Neha Gupta ◽  
Daniel J. Dooley ◽  
Steven Singh ◽  
Prakash Deedwania ◽  
...  

Author(s):  
Li Shen ◽  
Pardeep S. Jhund ◽  
Inder S. Anand ◽  
Peter E. Carson ◽  
Akshay S. Desai ◽  
...  

Abstract Background Sudden death (SD) and pump failure death (PFD) are leading modes of death in heart failure and preserved ejection fraction (HFpEF). Risk stratification for mode-specific death may aid in patient enrichment for new device trials in HFpEF. Methods Models were derived in 4116 patients in the Irbesartan in Heart Failure with Preserved Ejection Fraction trial (I-Preserve), using competing risks regression analysis. A series of models were built in a stepwise manner, and were validated in the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM)-Preserved and Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist (TOPCAT) trials. Results The clinical model for SD included older age, men, lower LVEF, higher heart rate, history of diabetes or myocardial infarction, and HF hospitalization within previous 6 months, all of which were associated with a higher SD risk. The clinical model predicting PFD included older age, men, lower LVEF or diastolic blood pressure, higher heart rate, and history of diabetes or atrial fibrillation, all for a higher PFD risk, and dyslipidaemia for a lower risk of PFD. In each model, the observed and predicted incidences were similar in each risk subgroup, suggesting good calibration. Model discrimination was good for SD and excellent for PFD with Harrell’s C of 0.71 (95% CI 0.68–0.75) and 0.78 (95% CI 0.75–0.82), respectively. Both models were robust in external validation. Adding ECG and biochemical parameters, model performance improved little in the derivation cohort but decreased in validation. Including NT-proBNP substantially increased discrimination of the SD model, and simplified the PFD model with marginal increase in discrimination. Conclusions The clinical models can predict risks for SD and PFD separately with good discrimination and calibration in HFpEF and are robust in external validation. Adding NT-proBNP further improved model performance. These models may help to identify high-risk individuals for device intervention in future trials. Clinical trial registration I-Preserve: ClinicalTrials.gov NCT00095238; TOPCAT: ClinicalTrials.gov NCT00094302; CHARM-Preserved: ClinicalTrials.gov NCT00634712. Graphic abstract


2012 ◽  
Vol 18 (8) ◽  
pp. S87
Author(s):  
Luke Cunningham ◽  
Anita Deswal ◽  
Wenyaw Chan ◽  
David Augilar ◽  
Biykem Bozkurt ◽  
...  

Author(s):  
Toshihide Izumida ◽  
Teruhiko Imamura ◽  
Takuya Fukui ◽  
Takatoshi Koi ◽  
Yohei Ueno ◽  
...  

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