Depression of systolic and diastolic myocardial reserve during atrial pacing tachycardia in patients with dilated cardiomyopathy.

Feldman, Marc D.; Alderman, James; Aroesty, Julian M.; Royal, Henry D.; Jj, Ferguson; Owen, Robert M.; Grossman, William; McKay, Raymond G.

doi:10.1172/jci113778

Cited by 160 publications

(60 citation statements)

References 32 publications

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“…Depressed cardiac contractility and impaired relaxation are key abnormalities contributing to morbidity and mortality in clinical HF (5,18). Despite the fact that numerous studies from both human (3,24) and animal (2, 22, 36) models of HF have attributed the mechanical dysfunction to changes in the calcium regulation observed in isolated myocytes (see Refs.…”

Section: Discussionmentioning

confidence: 99%

Spontaneous calcium release in tissue from the failing canine heart

Hoeker

Katra

Wilson

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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malities in calcium handling have been implicated as a significant source of electrical instability in heart failure (HF). While these abnormalities have been investigated extensively in isolated myocytes, how they manifest at the tissue level and trigger arrhythmias is not clear. We hypothesize that in HF, triggered activity (TA) is due to spontaneous calcium release from the sarcoplasmic reticulum that occurs in an aggregate of myocardial cells (an SRC) and that peak SCR amplitude is what determines whether TA will occur. Calcium and voltage optical mapping was performed in ventricular wedge preparations from canines with and without tachycardia-induced HF. In HF, steady-state calcium transients have reduced amplitude [135 vs. 170 ratiometric units (RU), P Ͻ 0.05] and increased duration (252 vs. 229 s, P Ͻ 0.05) compared with those of normal. Under control conditions and during ␤-adrenergic stimulation, TA was more frequent in HF (53% and 93%, respectively) compared with normal (0% and 55%, respectively, P Ͻ 0.025). The mechanism of arrhythmias was SCRs, leading to delayed afterdepolarization-mediated triggered beats. Interestingly, the rate of SCR rise was greater for events that triggered a beat (0.41 RU/ms) compared with those that did not (0.18 RU/ms, P Ͻ 0.001). In contrast, there was no difference in SCR amplitude between the two groups. In conclusion, TA in HF tissue is associated with abnormal calcium regulation and mediated by the spontaneous release of calcium from the sarcoplasmic reticulum in aggregates of myocardial cells (i.e., an SCR), but importantly, it is the rate of SCR rise rather than amplitude that was associated with TA. heart failure; arrhythmia; delayed afterdepolarization; triggered activity HEART FAILURE (HF) is a serious public health problem that afflicts millions of people in the United States alone (32). HF is associated with impaired cardiac contractility and relaxation, as well as a high incidence of ventricular arrhythmias and sudden death. Abnormal calcium handling has been implicated as a source of both mechanical and electrical dysfunction observed in HF, making it a key target for investigation and clinical therapy.At the myocyte level, impaired ventricular contractility and relaxation in HF have been attributed to decreased calcium transient amplitude due to diastolic sarcoplasmic reticulum (SR) calcium leak (12,13,35) and reduced SR calcium uptake (3,8,22,24). Calcium dysregulation in human HF has been associated with a significant incidence of nonreentrant arrhythmias (28,30,33) that can occur as the result of early afterdepolarizations (EADs) or delayed afterdepolarizations (DADs). At the subcellular level, a DAD is caused by spontaneous calcium release from the SR that activates a transient inward current with a magnitude that depends on the amount of calcium flux (33). While studies in isolated myocytes have provided valuable insight into cellular pathophysiology, the translation of these results to arrhythmogenesis at the tissue level is not straightforward.The fact...

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Section: Discussionmentioning

confidence: 99%

Spontaneous calcium release in tissue from the failing canine heart

Hoeker

Katra

Wilson

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…[32][33][34] Nevertheless, Sinha et al reported no adverse effects of long-term overdrive atrial pacing in patients with SA and HF. 22 In our study, mean nocturnal heart rate during OVP was of 71 ± 8 bpm with 96% ± 6% of ventricular pacing.…”

Section: Discussionmentioning

confidence: 99%

Overdrive Ventricular Pacing in Pacemaker Recipients with Permanent Atrial Fibrillation and Sleep Apnea

Bordier

Maurice-Tison

Ramana

2012

Journal of Clinical Sleep Medicine

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Study Objectives: Cardiac pacing is ineffective in obstructive sleep apnea (SA), but it can alleviate central SA/CheyneStokes respiration (CSA) in patients with heart failure (HF). We examined whether overnight overdrive ventricular pacing (OVP) has an effect on SA in pacemaker recipients with permanent atrial fi brillation (AF). Methods: An apnea-hypopnea index (AHI) ≥ 15 was confi rmed in 28/38 patients screened by fi nger pulse oximetry during overnight ventricular pacing at a backup rate of 40 bpm (BUV40). These patients (23 men, 77.9 ± 7.6 y, BMI 27.6 ± 5.1 kg/m 2 ) were randomly assigned to 2 consecutive nocturnal ventilation polygraphies with BUV40 versus OVP at 20 bpm above the mean nocturnal heart rate observed during screening. Results: During BUV40 versus OVP, (1) mean heart rate was 49 ± 8 versus 71 ± 8 bpm (p < 0.0001) and percent ventricular pacing 36% ± 38% versus 96% ± 6% (p < 0.0001); (2) AHI was 35.4 ± 11.9 versus 32.5 ± 15.5 (p = ns), central AHI 23.9 ± 11.8 versus 19.1 ± 12.7 (p < 0.001), and obstructive AHI 11.6 ± 13.1 versus 13.5 ± 15.9 (p = ns). In 15/28 patients without HF, mean left ventricular ejection fraction (LVEF) was 51% ± 17%, AHI was 37.6 ± 11.0 during BUV40 and 39.0 ± 11.5 during OVP, versus 32.8 ± 12.9 and 24.9 ± 16.5 in 13/28 patients with HF (p = 0.02) and mean LVEF 35% ± 15% (p = 0.01). Between the 2 subgroups, (1) central AHI was 23.6 ± 12.4 during BUV40 and 21.5 ± 14.0 during OVP versus 24.1 ± 11.6 and 16.2 ± 10.7 (p = 0.05); (2) obstructive AHI was 14.0 ± 13.7 during BUV40 and 17.6 ± 16.5 during OVP versus 8.8 ± 12.3 and 8.7 ± 14.3 (p = ns). Conclusions:The prevalence of SA, predominantly central, was high in our pacemaker recipients with permanent AF. In those with HF, a single overnight OVP resulted in modest improvement in central events. keywords: Heart failure, sleep apnea, atrial fi brillation, cardiac pacing Citation: Bordier P; Maurice-Tison S; Ramana NK. Overdrive ventricular pacing in pacemaker recipients with permanent atrial fi brillation and sleep apnea. S C I E N T I F I C I N V E S T I g A T I O N SA fter a fi rst report suggesting that cardiac pacing might alleviate sleep apnea (SA), subsequent studies have yielded confl icting results.1,2 An increase in pacing rate by overdrive atrial pacing, using a dual chamber pacemaker implanted for the treatment of bradycardia, has no effect on obstructive SA (OSA) in patients without history of heart failure (HF). In contrast, cardiac resynchronization therapy (CRT) does alleviate central SA/Cheyne-Stokes respiration (CSA), a breathing disorder present in > 30% of patients with stable HF and associated with a decreased survival rate. 3-14The aim of this study was to compare the effects of overnight overdrive ventricular pacing (OVP) versus overnight ventricular pacing at a low backup rate on SA in recipients of permanent pacemakers suffering from permanent atrial fi brillation (AF). The comparison was also made in separating the patients depending on whether they suffered from HF or not. Those patients were chosen ...

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“…On the other hand, reduced myocardial functional reserve during atrial pacing tachycardia or during dobutamine stress test is reportedly caused by the impairment of intracellular calcium handling, especially of SERCA2 or phospholamban (35)(36)(37) in the failing heart; and that is related to the poor prognosis (11,38 Fig. 1 and 2).…”

Section: Sympathetic Nerve Functional Imaging With 123 I-mibgmentioning

confidence: 99%

Nuclear Molecular Imaging of the Failing Heart

Ohshima

Isobe

Murohara

2018

Annals of Nuclear Cardiology

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Nuclear imaging of the failing myocardium is targeting the impaired part related to several processes of myocardial metabolism or work. Myocardium mainly utilizes fatty acid or glucose for ATP production in mitochondria. Intracellular calcium handling, which needs an amount of ATPs, induces myocardial contraction and relaxation, and is regulated with beta adrenal-stimulation. In the failing myocardium, any of these parts related to the myocardial work are variedly impaired, and could be the imaging target. Despite recent advancement of heart failure treatment, the patients with heart failure remain in high morbidity and mortality.For appropriate managements or prediction of prognosis in patients with heart failure, it is important to evaluate the mechanism of the failing myocardium. In this article, we focus on the usefulness of the 2 radionuclide imaging in evaluating sympathetic nerve function using myocardial 123 I-MIBG scintigraphy and mitochondrial function using myocardial 99m Tc-sestamibi SPECT in the patients with cardiomyopathy.

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Depression of systolic and diastolic myocardial reserve during atrial pacing tachycardia in patients with dilated cardiomyopathy.

Cited by 160 publications

References 32 publications

Spontaneous calcium release in tissue from the failing canine heart

Spontaneous calcium release in tissue from the failing canine heart

Overdrive Ventricular Pacing in Pacemaker Recipients with Permanent Atrial Fibrillation and Sleep Apnea

Nuclear Molecular Imaging of the Failing Heart

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