scholarly journals Atrial standstill in the newborn: a case report

2021 ◽  
Vol 26 (7) ◽  
pp. 4419
Author(s):  
O. Yu. Dzhaffarova ◽  
I. V. Plotnikova ◽  
L. I. Svintsova
Keyword(s):  
Heart Rate ◽  
Anticoagulant Therapy ◽  
Contractile Function ◽  
Electrophysiological Study ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Wide Complex Tachycardia ◽  
Ventricular Lead ◽  
Idioventricular Rhythm ◽  
Atrial Enlargement

Introduction. Persistent atrial standstill is a rare syndrome characterized by absence of mechanical and electrical atrial activity. The article presents a unique case of atrial standstill in the newborn patient with tachyarrhythmia.Brief description. The first manifestation of atrial standstill in the patient was heart failure (HF) manifestations and wide-complex tachycardia according to electrocardiography, which was identified as ventricular tachycardia. At the local outpatient clinic, the child was prescribed with antiarrhythmic therapy (AAT), which decreased heart rate. Three months later, a transesophageal electrophysiological study was carried out in our center in order to determine the arrhythmia origin. A multiform idioventricular rhythm with a heart rate of 46-119 beats per min was diagnosed, atrial pacing spike (A waves) was not recorded. Given bradyarrhythmia, hemodynamic abnormalities on echocardiography (significant atrial enlargement, decreased contractility), the patient, in order to prevent the risk of sudden cardiac death, underwent implantation of single chamber pacemaker in VVIR mode and bipolar ventricular lead. Anticoagulant therapy was prescribed. After 6-month follow-up, relief of HF symptoms and an increase in left ventricular contractile function was noted.Discussion. Timely diagnosis and implantation of pacemakers allowed avoiding AAT and minimizing the HF symptoms. Continuous ventricular pacing and anticoagulant therapy are important in HF prevention.

scholarly journals Heart Rate–Induced Myocardial Ca 2+ Retention and Left Ventricular Volume Loss in Patients With Heart Failure With Preserved Ejection Fraction

2020 ◽  
Vol 9 (17) ◽  
Author(s):  
Daniel N. Silverman ◽  
Mehdi Rambod ◽  
Daniel L. Lustgarten ◽  
Robert Lobel ◽  
Martin M. LeWinter ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Sinus Rhythm ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Preserved Ejection Fraction ◽  
Volume Loss ◽  
Heart Rates ◽  
Patients With Heart Failure

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.

scholarly journals Overexpression of A3 adenosine receptors decreases heart rate, preserves energetics, and protects ischemic hearts

2002 ◽  
Vol 283 (4) ◽  
pp. H1562-H1568 ◽  
Author(s):  
Heather R. Cross ◽  
Elizabeth Murphy ◽  
Richard G. Black ◽  
John Auchampach ◽  
Charles Steenbergen
Keyword(s):  
Heart Rate ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Specific Inhibitor ◽  
Left Ventricular ◽  
Atp Depletion ◽  
Wild Type ◽  
Basal Heart Rate ◽  
Developed Pressure

To determine whether A3 adenosine receptor (A3AR) signaling modulates myocardial function, energetics, and cardioprotection, hearts from wild-type and A3AR-overexpressor mice were subjected to 20-min ischemia and 40-min reperfusion while 31P NMR spectra were acquired. Basal heart rate and left ventricular developed pressure (LVDP) were lower in A3AR-overexpressor hearts than wild-type hearts. Ischemic ATP depletion was delayed and postischemic recoveries of contractile function, ATP, and phosphocreatine were greater in A3AR-hearts. To determine the role of depressed heart rate and to confirm A3AR-specific signaling, hearts were paced at 480 beats/min with or without 60 nmol/l MRS-1220 (A3AR-specific inhibitor) and then subjected to ischemia-reperfusion. LVDP was similar in paced A3AR-overexpressor and paced wild-type hearts. Differences in ischemic ATP depletion and postischemic contractile and energetic dysfunction remained in paced A3AR-overexpressor hearts versus paced wild-type hearts but were abolished by MRS-1220. In summary, A3AR overexpression decreased basal heart rate and contractility, preserved ischemic ATP, and decreased postischemic dysfunction. Pacing abolished the decreased contractility but not the ATP preservation or cardioprotection. Therefore, A3AR overexpression results in cardioprotection via a specific A3AR effect, possibly involving preservation of ATP during ischemia.

Hypertrophic Cardiomyopathy: Non-Invasive Assessment of Diastolic and Systolic Functional Parameters in Relation to Heart Rate

1985 ◽  
Vol 24 (05) ◽  
pp. 196-200
Author(s):  
R. P. Spielmann ◽  
M. Geiger ◽  
A. Clausen ◽  
K.-H. Kuck ◽  
R. Montz ◽  
...  
Keyword(s):  
Heart Rate ◽  
Hypertrophic Cardiomyopathy ◽  
Radionuclide Ventriculography ◽  
Left Ventricular ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Heart Rates ◽  
Ventricular Compliance ◽  
The Individual ◽  
Left Ventricular Compliance

SummaryHypertrophic cardiomyopathy (HC) is characterized by reduced left ventricular compliance and subsequent filling abnormalities. To study the pathophysiologic changes in parameters of left ventricular systolic and diastolic performance as a function of increasing heart rate 14 patients with HC (32 ± 12 yrs; 11 M, 4 F) and 4 normal individuals were subjected to equilibrium radionuclide ventriculography (99mTc-labelled red blood cells) at rest and during incremental right atrial pacing; heart rate was increased in steps of 20 beats per min from basal state to the individual symptom-limited endpoint. Mean symptom-limited heart rate was 141 ± 28 in HC and 160 in normals (p <.01.). At each pacing level filling and ejection parameters as well as the left ventricular endsystolic (LVESV) and enddiastolic volume (LVEDV) were determined relative to resting volumes at a heart rate of 78 ± 8. At the individual maximal pacing rate HC revealed a decline in LVEDV to 61 ± 4 % (p C.001) and an increase in LVESV to 117 ± 14% (p <.001) resulting in decreasing ejection fractions at heart rates above 120. Peak LV filling rates initially increased but subsequently decreased steeply at heart rates above 100; peak LV ejection rates in HC showed a similar pattern with increasing frequency. Time inter- vais to peak ejection and peak filling rate did not differ from normal. Thus, patients with HC demonstrated combined left ventricular diastolic and systolic abnormalities with increasing heart rate leading into a low-input low-output circulatory state. This probably explains not only the symptoms associated with HC, but also supports the concept of “hemodynamic syncope” in HC.

Modulation of force-frequency relation by phospholamban in genetically engineered mice

1999 ◽  
Vol 276 (6) ◽  
pp. H2245-H2250 ◽  
Author(s):  
Vivek J. Kadambi ◽  
Nancy Ball ◽  
Evangelia G. Kranias ◽  
Richard A. Walsh ◽  
Brian D. Hoit
Keyword(s):  
Heart Rate ◽  
Myocardial Contractility ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Force Frequency ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Peak Rate ◽  
Genetically Engineered Mice ◽  
Frequency Relation

Phospholamban levels regulate cardiac sarcoplasmic reticulum Ca2+ pump activity and myocardial contractility. To determine whether and to what extent phospholamban modulates the force-frequency relation and ventricular relaxation in vivo, we studied transgenic mice overexpressing phospholamban (PLBOE), gene-targeted mice without phospholamban (PLBKO), and isogenic wild-type controls. Contractility was assessed by the peak rate of left ventricular (LV) isovolumic contraction (+dP/d t max), and diastolic function was assessed by both the peak rate (−dP/d t max) and the time constant (τ) of isovolumic LV relaxation, using a high-fidelity LV catheter. Incremental atrial pacing was used to generate heart rate vs. −dP/d t max(force-frequency) relations. Biphasic force-frequency relations were produced in all animals, and the critical heart rate (HRcrit) was taken as the heart rate at which dP/d t max was maximal. The average LV +dP/d t maxincreased in both PLBKO and PLBOE compared with their isogenic controls (both P < 0.05). The HRcrit for LV +dP/d t max was significantly higher in PLBKO (427 ± 20 beats/min) compared with controls (360 ± 18 beats/min), whereas the HRcrit in PLBOE (340 ± 30 beats/min) was significantly lower compared with that in isogenic controls (440 ± 25 beats/min). The intrinsic heart rates were significantly lower, and the HRcrit and the ±dP/d t max at HRcrit were significantly greater in FVB/N than in SvJ control mice. We conclude that 1) the level of phospholamban is a critical negative determinant of the force-frequency relation and myocardial contractility in vivo, and 2) contractile parameters may differ significantly between strains of normal mice.

Abstract MP209: Troponin I Phosphorylation Is Essential For Cardiac Reserve

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Sarah L Sturgill ◽  
Lorien G Salyer ◽  
Vikram Shettigar ◽  
Elizabeth Brundage ◽  
Brandon J Biesiadecki ◽  
...  
Keyword(s):  
Heart Rate ◽  
Strain Rate ◽  
Diastolic Function ◽  
Troponin I ◽  
Contractile Function ◽  
Radial Strain ◽  
Left Ventricular ◽  
Resting Heart Rate ◽  
Cardiac Reserve ◽  
Systolic And Diastolic Function

In response to increase in metabolic demand (e.g., exercise), the heart must increase its pumping performance to meet this demand. To achieve this increase, the heart relies on its cardiac reserve, which is the ability to increase in its contractile and diastolic function. The mechanism responsible for cardiac reserve is poorly understood. The myofilament is the mechanism responsible for contraction and relaxation. Troponin I (the inhibitory subunit of troponin, TnI) is a key regulatory protein. Studies have shown TnI serine 23/24 (S23/S24) phosphorylation, the most abundant and important TnI phosphorylation, is a key mechanism for accelerating relaxation by decreasing Ca 2+ senstivity. The role of TnI in cardiac reserve is unknown. For this study, we thoroughly characterized the systolic and diastolic reserve in TnI S23/S24 phosphorylation-null transgenic mice (S23/S24 mutated to alanine, AA mice). Even with increased Ca 2+ sensitivity, the AA mice exhibited normal function at resting heart rate and no difference in cardiac structure compared to wildtype. To increase in vivo heart performance, the most important system is the Bowditch effect (i.e., an increase in contractile function with increasing heart rate). To examine the role TnI S23/S24 phosphorylation in systolic and diastolic reserve, we assessed hemodynamics via left ventricular catheterization on the Bowditch effect by increasing heart rate from 240 to 420 beats per minute. Our data exhibited a clear loss of diastolic and systolic reserve in the AA mice. Since we observed a clear inability to increase systolic and diastolic function in AA mice, we performed speckle tracking echocardiography to more quantitatively investigate AA mice function. We observed that AA mice demonstrated normal systolic function (radial strain rate) and impaired directional diastolic function (reverse radial strain rate) at resting heart rate. We conclude that TnI S23/S24 phosphorylation is essential for cardiac reserve by enhancing systolic and diastolic function. A blunted cardiac reserve leads to heart disease making TnI S23/S24 phosphorylation a potential therapeutic strategy.

Relation of glycosylated hemoglobin to in vivo cardiac function in response to dobutamine in spontaneously diabetic BB Wor rats

1994 ◽  
Vol 72 (7) ◽  
pp. 722-727 ◽  
Author(s):  
Tom L. Broderick ◽  
Stephen J. Kopp ◽  
June T. Daar ◽  
Fred D. Romano ◽  
Dennis J. Paulson
Keyword(s):  
Heart Rate ◽  
Cardiac Function ◽  
Metabolic Control ◽  
Contractile Function ◽  
Glycosylated Hemoglobin ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Insulin Dependent ◽  
Myocardial Contractile

The contribution of metabolic control to in vivo myocardial contractile function in response to β1-adrenergic stimulation was determined in the spontaneously diabetic BB Wor rat. The study involved a group of insulin-dependent BB Wor rats showing marked variations in metabolic control, assessed by the level of glycosylated hemoglobin (gHb). These diabetic BB rats were divided into moderate and severe (%gHb > 14) diabetic groups. A group of Wistar rats and diabetes-resistant BB Wor rats served as controls. In vivo myocardial contractile function was measured under basal conditions and after i.v. dobutamine infusions in anesthetized rats, using a catheter-tip pressure transducer inserted into the left ventricle. No dramatic differences in heart rate with dobutamine stimulation were observed between the moderate, severe diabetic, and diabetes-resistant groups. However, heart rate was lower in Wistar control rats compared with these groups. Systolic left ventricular pressure was depressed in severe diabetic rats compared with Wistar controls. In addition, positive dP/dt was significantly less in the severe diabetic group at the highest doses of stimulation, whereas negative dP/dt was depressed under basal conditions and remained so with increasing doses of dobutamine. In the diabetic group maximal systolic left ventricular pressure, rate–pressure product, and negative dP/dt responses to dobutamine were all inversely correlated with gHb. These results indicate that changes in metabolic control of the insulin-dependent BB diabetic rat can contribute to a depressed myocardial contractile function.Key words: glycosylated hemoglobin, cardiac function, dobutamine, BB rat.

Contractile function and myofibrillar ATPase activity in the exercise-trained dog heart

1977 ◽  
Vol 43 (6) ◽  
pp. 977-982 ◽  
Author(s):  
R. T. Dowell ◽  
H. L. Stone ◽  
L. A. Sordahl ◽  
G. K. Asimakis
Keyword(s):  
Heart Rate ◽  
Exercise Training ◽  
Atpase Activity ◽  
Contractile Function ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Submaximal Exercise ◽  
Treadmill Running ◽  
Myofibrillar Atpase ◽  
Myofibrillar Atpase Activity

Myocardial contractility and the enzymatic (ATPase) activity of cardiac contractile proteins were examined after exercise training using the chronically instrumented, unanesthetized dog as an experimental model. Before training, heart rate and the maximum rate of left ventricular pressure development (max dP/dt) were measured at rest and during submaximal exercise. Animals were then subjected to an 8- to 10-wk treadmill running program. Training was verified by the establishment of a 10- to 20-beat/min reduction in heart rate during submaximal exercise. After training max dP/dt was within normal limits at rest, but significantly elevated during submaximal exercise. When max dP/dt was plotted as a function of heart rate, either with the animal standing quietly on the treadmill or during submaximal exercise, a marked elevation in max dP/dt at any given heart rate was observed following training. Myofibrillar protein yield and ATPase activity values were nearly identical in left ventricles from exercise-trained and sedentary control dogs. Although exercise training by treadmill running improved contractile function in the unanesthetized dog myocardium, this response does not appear to involve alterations in myofibrillar ATPase activity.

Activation time of myocardial oxidative phosphorylation in creatine kinase and adenylate kinase knockout mice

2002 ◽  
Vol 282 (6) ◽  
pp. H2259-H2264 ◽  
Author(s):  
Lori A. Gustafson ◽  
Johannes H. G. M. Van Beek
Keyword(s):  
Heart Rate ◽  
Creatine Kinase ◽  
Oxygen Consumption ◽  
Response Time ◽  
Adenylate Kinase ◽  
Contractile Function ◽  
Left Ventricular ◽  
Wild Type ◽  
Dynamic Regulation ◽  
Developed Pressure

Our goal was to determine whether mice genetically altered to lack either creatine kinase (M/MtCK−/−) or adenylate kinase (AK−/−) show altered properties in the dynamic regulation of myocardial oxygen consumption (MV˙o 2). We measured contractile function, oxygen consumption, and the mean response time of oxygen consumption to a step increase in heart rate [i.e., mitochondrial response time ( t mito)] in isolated Langendorff-perfused hearts from wild-type ( n = 6), M/MtCK−/− ( n = 6), and AK−/− ( n = 4) mice. Left ventricular developed pressure was higher in M/MtCK−/− hearts (88.2 ± 6.8 mmHg) and lower in AK−/− hearts (46.7 ± 9.4 mmHg) compared with wild-type hearts (60.7 ± 10.1 mmHg) at the basal pacing rate. Developed pressure fell slightly when heart rate was increased in all three groups. Basal MV˙o 2 at 300 beats/min was 19.1 ± 2.4, 19.4 ± 1.5, and 16.3 ± 1.9 μmol · min−1 · g dry wt−1for M/MtCK−/−, AK−/−, and wild type, respectively, which increased to 25.5 ± 3.7, 25.4 ± 2.6, and 22.0 ± 2.6 μmol · min−1 · g−1, when heart rate was increased to 400 beats/min. The t mito was significantly faster in M/MtCK−/− hearts: 3.0 ± 0.3 versus 7.3 ± 0.6 and 8.0 ± 0.4 s for M/MtCK−/−, AK−/−, and wild-type hearts, respectively. Our results demonstrate that MV˙o 2 of M/MtCK−/− hearts adapts more quickly to an increase in heart rate and thereby support the hypothesis that creatine kinase acts as an energy buffer in the cytosol, which delays the energy-related signal between sites of ATP hydrolysis and mitochondria.

Effects of asynchrony on myocardial relaxation at rest and during exercise in conscious dogs

1988 ◽  
Vol 254 (5) ◽  
pp. H817-H822 ◽  
Author(s):  
G. R. Heyndrickx ◽  
P. J. Vantrimpont ◽  
M. F. Rousseau ◽  
H. Pouleur
Keyword(s):  
Heart Rate ◽  
Right Ventricular ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Ventricular Pacing ◽  
Right Ventricular Pacing ◽  
Relaxation Phase

The effect of left ventricular asynchrony induced by right ventricular pacing on relaxation indexes was studied at rest and during exercise in seven conscious dogs instrumented for chronic measurements of left ventricular pressure, coronary blood flow, and arterial pressure and with right atrial and ventricular pacing electrodes. Increasing heart rate with atrial pacing resulted in an increase in both left ventricular maximum and minimum rates of pressure development, LV dP/dtmax and LV dP/dtmin, respectively, as well as in a decrease in the relaxation constant T. In contrast, increasing heart rate with ventricular pacing resulted in a decrease in LV dP/dtmax, a small increase in LV dP/dtmin, and a significant decrease in T. During exercise with heart rate kept constant with atrial pacing, both LV dP/dtmax and LV dP/dtmin increased and T decreased to the same extent as during exercise in sinus rhythm. In contrast, exercising during right ventricular pacing resulted in a significant increase in T, expressing a slowing of relaxation. It is concluded that increasing heart rate alone in the presence of asynchrony of LV contraction induced by abnormal electrical activation results in a depressed contractile response, while the relaxation phase is not significantly affected. However, during sympathetic stimulation, a condition where synchronization should be improved, the relaxation phase is considerably lengthened.

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