ライフサイエンスコーパス: arrhythmia

1 he first described and most common inherited arrhythmia.

2 medication/nonadherence and supraventricular arrhythmia.

3 ction which could lead to increased risk for arrhythmia.

4 therapies or on the basis of ECG-documented arrhythmia.

5 ggering heart failure-associated ventricular arrhythmia.

6 electrophysiology services for patients with arrhythmia.

7 for the prevention or therapy of this common arrhythmia.

8 was life-threatening hypotension or cardiac arrhythmia.

9 ongation is an accepted surrogate marker for arrhythmia.

10 onic current for termination of the detected arrhythmia.

11 iorates heart failure-associated ventricular arrhythmia.

12 nce of spontaneous and sustained ventricular arrhythmia.

13 cluding epileptic encephalopathy and cardiac arrhythmia.

14 veloped as therapeutics for LQTS and cardiac arrhythmia.

15 lowing treatment guidelines for the specific arrhythmia.

16 ial fibrillation (AF) is a common and morbid arrhythmia.

17 conduction delay and spontaneous episodes of arrhythmia.

18 genetic risk factors that contribute to the arrhythmia.

19 venting heart failure-associated ventricular arrhythmia.

20 th atrial fibrillation (AF), the most common arrhythmia.

21 epolarization, which associates with cardiac arrhythmia.

22 underscores asynchronous Ca(2+) release and arrhythmia.

23 disease, heart failure, stroke, and cardiac arrhythmias.

24 associated with life-threatening ventricular arrhythmias.

25 g (SDB) is frequently associated with atrial arrhythmias.

26 to the initiation and maintenance of atrial arrhythmias.

27 ation, and/or occurrence of life-threatening arrhythmias.

28 e (LQTS) are predisposed to life-threatening arrhythmias.

29 associated with an increased risk of cardiac arrhythmias.

30 tion (LVEF) face a high risk for ventricular arrhythmias.

31 s)-bundle associated with lethal ventricular arrhythmias.

32 tion of cellular dysfunction, apoptosis, and arrhythmias.

33 because of hypertension or supraventricular arrhythmias.

34 pecies signals can prevent calcium-dependent arrhythmias.

35 mice displayed atrial conduction disease and arrhythmias.

36 ardial infarction, heart failure and cardiac arrhythmias.

37 tivation, inactivation, ion selectivity, and arrhythmias.

38 usceptibility to burst pacing-induced atrial arrhythmias.

39 l activity once disturbed, as with sustained arrhythmias.

40 eltaC transgenic mice rapidly develop HF and arrhythmias.

41 unction, and a high incidence of ventricular arrhythmias.

42 nary artery disease, myocardial fibrosis and arrhythmias.

43 to guide treatment of ventricular ectopy and arrhythmias.

44 rial fibrillation and other types of cardiac arrhythmias.

45 pendent effect that may increase the risk of arrhythmias.

46 sfunctions and should be considered to treat arrhythmias.

47 nces and associations with heart failure and arrhythmias.

48 potential that can trigger fatal ventricular arrhythmias.

49 eatment altered the incidence of reperfusion arrhythmias.

50 and death from heart failure or ventricular arrhythmias.

51 of mice resulted in SAN hypoplasia and sinus arrhythmias.

52 isolation, and freedom from recurrent atrial arrhythmias.

53 Clonidine suppressed SNA and abolished all arrhythmias.

54 malizing X-ROS can prevent Ca(2+) -dependent arrhythmias.

55 cting calsequestrin mutations provoke lethal arrhythmias.

56 atrium (LA) that begets atrial myopathy and arrhythmias.

57 therapies against heart failure and cardiac arrhythmias.

58 ecular mechanism for some lethal ventricular arrhythmias.

59 tricular action potential and causes cardiac arrhythmias.

60 T prolongation leading to lethal ventricular arrhythmias.

61 advanced heart failure, and life-threatening arrhythmias.

62 ct region as source and substrate of post-MI arrhythmias.

63 ratio, 2.48; 95% CI, 1.62 to 3.79), cardiac arrhythmia (11.5%, vs. 5.6% among those without arrhythm

64 ] vs 33 [2.5%]) and supraventricular cardiac arrhythmia (12 [0.9%] vs 13 [1.0%]).

65 ere hospitalized for symptomatic ventricular arrhythmia (19.5% versus 25.3%; P=0.27).

66 Common complications were arrhythmias (19%), cardiac arrest (10%), sepsis (7%), an

67 s syndrome (25%), neurological events (25%), arrhythmias (22%), and venous thromboembolism (9%).

68 atients with MVP and comprehensive clinical, arrhythmia (24-h Holter monitoring) and Doppler-echocard

69 here were no differences in post LVAD atrial arrhythmias (AA) (Adjusted OR = 0.45 [0.18-1.06], p = 0.

70 All patients had current guidelines arrhythmia ablation indication.

71 cker was Torsades de Pointes (TdP) reentrant arrhythmia activations in 100% of tested monolayers.

72 19 itself can also induce myocardial injury, arrhythmia, acute coronary syndrome and venous thromboem

73 ic complications, myocardial dysfunction and arrhythmia, acute coronary syndromes, acute kidney injur

74 rillation (AF) is a highly prevalent cardiac arrhythmia and cause of significant morbidity and mortal

75 int was a composite of malignant ventricular arrhythmia and end-stage heart failure.

76 utations in HCN channels are linked to heart arrhythmia and epilepsy.

77 The risk of arrhythmia and heart failure was comparable among sexes.

78 been linked to cardiac pathologies including arrhythmia and heart failure.

79 on (AF) is the most common sustained cardiac arrhythmia and is a major cause of stroke and morbidity.

80 llation is the most common sustained cardiac arrhythmia and is associated with considerable morbidity

81 ibrillation (AF) is the most common clinical arrhythmia and is associated with heart failure, stroke,

82 Atrial fibrillation (AF) is the most common arrhythmia and is associated with inflammation.

83 ention of QT prolongation, ventricular tachy-arrhythmias and cardiac arrest.

84 opment of various cardiac disorders (such as arrhythmias and cardiomyopathy) and circulatory complica

85 are associated with adverse outcomes such as arrhythmias and death.

86 c Ca(2+) leak from the SR that both triggers arrhythmias and impairs contractility.

87 Awareness of drugs that may cause arrhythmias and knowledge of distinct arrhythmias that m

88 2, which have been reported to cause cardiac arrhythmias and reduced conduction.

89 investigates the association between cardiac arrhythmias and short-term exposures to fine particulate

90 gy that could increase the susceptibility to arrhythmias and sudden cardiac death in HD patients.

91 failing hearts, contributing to ventricular arrhythmias and sudden cardiac death.

92 mplicated in the pathogenesis of ventricular arrhythmias and sudden cardiac death.

93 dromes associated with malignant ventricular arrhythmias and sudden cardiac death.

94 , potentially increasing the risk of cardiac arrhythmias and sudden death.

95 g QT syndrome, which can lead to ventricular arrhythmias and sudden death.

96 ase the risk of fentanyl-induced ventricular arrhythmias and sudden death.

97 tous therapy and pharmacotherapy for cardiac arrhythmias and/or heart failure in addition to device p

98 ion, coronary artery dilation and aneurysms, arrhythmia, and conduction abnormalities.

99 duce behavioral quiescence and rest-activity arrhythmia, and facilitate recovery of cellular homeosta

100 al opacities, testicular maldescent, cardiac arrhythmia, and higher rates of developmental and mood d

101 sed clinically for the treatment of malaria, arrhythmia, and pseudobulbar effect, quinidine can induc

102 eports of patients with myocardial ischemia, arrhythmia, and sudden cardiac death.

103 including that of thromboembolic disease and arrhythmia, and to discuss their clinical sequelae.

104 e composite of ICD implantation, ventricular arrhythmias, and cardiac arrest: 0.96% (95% CI: 0.77% to

105 ing Brugada syndrome, idiopathic ventricular arrhythmias, and epileptic encephalopathy.

106 diac injury with cardiomyopathy, ventricular arrhythmias, and hemodynamic instability in the absence

107 e of myocardial ischemia, occurrence rate of arrhythmias, and length of ICU stay were observed.

108 ts as dilated cardiomyopathy, heart failure, arrhythmias, and sudden death.

109 were cardiac death or arrest, heart failure, arrhythmias, and urgent interventions.

110 luding acute myocardial injury, myocarditis, arrhythmias, and venous thromboembolism.

111 iomarker for patients at risk of ventricular arrhythmias, and we have learned of the potential role o

112 Ventricular arrhythmias are a major early complication after myocard

113 It is now established that the deadly arrhythmias are caused by unregulated 'pathological' cal

114 amounts of circulating cytokines and cardiac arrhythmias are demonstrated along with a frequent conco

115 The main inherited cardiac arrhythmias are long QT syndrome, short QT syndrome, cat

116 studies have shown that SCD and ventricular arrhythmias are more likely to occur in the morning than

117 equent arrhythmia, but malignant ventricular arrhythmias are most commonly associated with severe LVS

118 All these arrhythmias are potentially life-threatening and have su

119 Mechanisms of arrhythmias are well known for some medications but, in

120 Cardiomyopathy features, heart failure and arrhythmia, are similar among the sexes.

121 Life-threatening cardiac arrhythmias arise from asynchrony in these space-time ev

122 These arrhythmias, arising from catecholamine excess rather th

123 prolongation, which may lead to ventricular arrhythmias as a possible explanation of this increased

124 s in calmodulin associated with two distinct arrhythmias as well as two different neurodegenerative d

125 We recently sequenced 35 arrhythmia-associated genes from 70 unexplained stillbir

126 ions, and incidence of sustained ventricular arrhythmias at 24 months.

127 lar complexes and pacing-induced ventricular arrhythmias at ZT14, and the hearts at ZT14 had diminish

128 tion of such patients diagnosed with cardiac arrhythmia attributable to the medications is 47 per 100

129 to i) discriminate between normal rhythm and arrhythmia based on frequency-dependent gating and ii) g

130 thodology for both heart failure and cardiac arrhythmias because the confidence intervals overlap bet

131 Additionally, it intends to investigate the arrhythmias behavior after cardioneuroablation.

132 Some drug-induced arrhythmias (bradyarrhythmias, atrial tachycardia, atrio

133 thyl flecainide had no significant effect on arrhythmia burden, despite comparable sodium channel blo

134 , heart transplantation, device therapies or arrhythmia burden.

135 TTNtv is characterized by frequent arrhythmia, but malignant ventricular arrhythmias are mo

136 rge cohort of patients with MVP, ventricular arrhythmia by Holter monitoring was frequent but rarely

137 in the heart can acutely promote ventricular arrhythmias by disrupting ventricular myocyte intercalat

138 predispose otherwise normal hearts to atrial arrhythmias by dynamically disrupting Na(V)1.5-rich ID n

139 disorders, has been associated with obesity, arrhythmias, cardiac ischemia, insulin resistance, etc.

140 lsequestrin cause the highly lethal familial arrhythmia catecholaminergic polymorphic ventricular tac

141 12-lead ECGs from 40,258 patients with four arrhythmia classes: atrial fibrillation, general suprave

142 The proposed optimal multi-stage arrhythmia classification approach can dramatically bene

143 ave jointly optimized the entire multi-stage arrhythmia classification scheme based on 12-lead surfac

144 creased in rats paced with respiratory sinus arrhythmia compared to monotonic pacing, via improvement

145 ncluded cardiac death or arrest, ventricular arrhythmias, congestive heart failure or arrhythmias req

146 ants associated with MCVD (cardiomyopathies, arrhythmias, connective tissue disorders, and familial h

147 Arrhythmia constitutes a problem with the rate or rhythm

148 ) using an external validation data, MIT-BIH arrhythmia database.

149 Overall mortality after arrhythmia diagnosis (8 years; 13 +/- 2%) was strongly a

150 ase myocardial oxygen consumption and induce arrhythmias, diastolic hypotension may reduce coronary p

151 kout syndrome (TKOS) is a potentially lethal arrhythmia disorder caused by recessively inherited null

152 device have thus far excluded patients with arrhythmias due to the potential effect of arrhythmias o

153 ith an increased risk of de-novo ventricular arrhythmia during hospitalisation.

154 roperties that are appealing for noninvasive arrhythmia elimination.

155 brillation (AF) is the most common sustained arrhythmia encountered in humans and is a significant so

156 Malignant ventricular arrhythmia end points most commonly occurred in patients

157 [CI]: 1.27 to 5.77; p = 0.01 vs. no/trivial arrhythmia), even after it was comprehensively adjusted,

158 improved cardiac function; abrogated cardiac arrhythmias, fibrosis, and apoptosis; and prolonged the

159 dysfunction, conduction defect, ventricular arrhythmias, fibrosis, apoptosis, and premature death wi

160 strongly associated with severe ventricular arrhythmias for DSP cases (P<0.001, sensitivity 85%, spe

161 ion fraction <45% was associated with severe arrhythmias for PKP2 cases (P<0.001) but was poorly asso

162 Cardiac volumes, arrhythmias, function and remodeling were determined at

163 ing diagnoses of coronary artery disease and arrhythmia had the highest likelihood of cardiac surveil

164 Life threatening arrhythmias have an incidence of 3.6% and were associate

165 Cardiac arrhythmias, heart failure, and nonfatal coronary syndro

166 coronary artery disease in 25%, ventricular arrhythmia history in 1.4%, and no significant comorbidi

167 se (HR: 1.89; 95% CI: 1.26 to 2.82), cardiac arrhythmias (HR: 1.62; 95% CI: 1.28 to 2.05), chronic ki

168 Cardiac arrhythmias (i.e. inappropriate sinus tachycardia and br

169 Bailout ablation for refractory ventricular arrhythmia in cardiogenic shock allowed successful weani

170 on (AF) is the most common sustained cardiac arrhythmia in clinical practice and is known to be assoc

171 inct mechanisms underlie hypokalemia-induced arrhythmia in the ventricle and atrium but also vary bet

172 ase the risk of life-threatening ventricular arrhythmia in these patients.

173 nnel function and this may precipitate fatal arrhythmia in utero.

174 trategy for preventing heart dysfunction and arrhythmias in DMD patients.

175 ventions to mitigate cardiac dysfunction and arrhythmias in DMD patients.

176 hat it may explain the propensity for atrial arrhythmias in HF.

177 e to dangerous pathological states including arrhythmias in infected hearts.

178 olarization and most importantly to suppress arrhythmias in LQTS2.

179 The risks of thromboembolism and ventricular arrhythmias in LVNC patients were similar to dilated car

180 fusion (I-R) are major causes of ventricular arrhythmias in patients with a history of coronary arter

181 ict the 5-year risk of malignant ventricular arrhythmias in patients with ARVC.

182 iated with higher rates of heart failure and arrhythmias in patients with HCM.

183 may be useful for prevention or treatment of arrhythmias in SDB.

184 st ischaemia-induced and reperfusion-induced arrhythmias in the adult myocardium, and compares the ef

185 died the mechanisms triggering these post-MI arrhythmias in vivo and their relation to regional myocy

186 s in AAA cardiomyocytes and the incidence of arrhythmias in vivo compared with the controls.

187 s when the principal provoking mechanism was arrhythmia, in comparison with postoperative status, hyp

188 0 min), followed by reperfusion (2 min), and arrhythmia incidence quantified.

189 Management of drug-induced arrhythmias includes discontinuation of the offending me

190 s the fact that drugs can also trigger other arrhythmias, including bradyarrhythmias, atrial fibrilla

191 rotein calmodulin (CaM) cause severe cardiac arrhythmias, including catecholaminergic polymorphic ven

192 ct zone forms a substrate for re-entry while arrhythmia initiation is often associated with sympathet

193 aging confounders were minimized by using an arrhythmia-insensitive-rapid (AIR) cardiac T1 mapping pu

194 ft ventricular dysfunction, heart failure or arrhythmia is associated with a poor prognosis.

195 This multifactorial arrhythmia is intertwined with common concomitant cardio

196 Respiratory sinus arrhythmia is physiological pacing of the heart that dis

197 is of the electrophysiological substrate for arrhythmias is crucial for optimal risk stratification.

198 nfections, the risk of malignant ventricular arrhythmias is increased, partly because of a higher pro

199 Atrial fibrillation, the most common cardiac arrhythmia, is an important contributor to mortality and

200 tion (AF), the most common sustained cardiac arrhythmia, is associated with substantial morbidity, mo

201 TA6, whose mutations in humans are linked to arrhythmia, is highly expressed in the SAN and its haplo

202 brillation (AF) is an increasingly prevalent arrhythmia; its pathophysiology and progression are well

203 Prolonged QTc interval and life-threatening arrhythmias (LTA) are potential drug induced complicatio

204 the efficacy of drugs targeting EAD-mediated arrhythmias may depend on the time of day that they are

205 This model clarifies a heretofore unknown arrhythmia mechanism and extends our understanding of tr

206 ; however, little is known of the underlying arrhythmia mechanism.

207 en numerous advances in our understanding of arrhythmia mechanisms, diagnosis, and new therapies.

208 to the fundamental cellular and tissue-level arrhythmia mechanisms.

209 OVID-19 who die experience malignant cardiac arrhythmias more often than those surviving to discharge

210 Arrhythmia mutation sites undergo large translocations d

211 COVID-19 can have both primary (arrhythmias, myocardial infarction, and myocarditis) and

212 The most common forms of CVD included arrhythmia (n = 88, 28.8%), congenital heart disease (n

213 In patients with life-threatening arrhythmias necessitating ICD implantation, we compared

214 ty and the occurrence of de-novo ventricular arrhythmias (non-sustained or sustained ventricular tach

215 fects reported with ADHD stimulants included arrhythmia, nonischemic cardiomyopathy, Takotsubo cardio

216 Cardiac gene expression and arrhythmia occurrence have time-of-day variation; howeve

217 hythmia (11.5%, vs. 5.6% among those without arrhythmia; odds ratio, 1.95; 95% CI, 1.33 to 2.86), chr

218 and vasculature can cause potentially lethal arrhythmias, often in the setting of comorbid blood pres

219 h arrhythmias due to the potential effect of arrhythmias on the peripheral arterial tonometry (PAT) a

220 ial (p = 0.0003) and ventricular (p = 0.009) arrhythmia onset.

221 ly for 2 weeks with either respiratory sinus arrhythmia or paced monotonically at a matched heart rat

222 heart rate variability is respiratory sinus arrhythmia or RSA - an intrinsic respiratory modulated p

223 not reduce mortality or hospitalization for arrhythmia or worsening heart failure during 1 year of f

224 have seen at least one patient for inherited arrhythmias or cardiomyopathies.

225 0.45 [0.18-1.06], p = 0.31) and ventricular arrhythmias (OR = 0.65 [0.41-1.78], p = 0.41).

226 ced the incidence of acute ischaemia-induced arrhythmias (p = 0.028), with a reduction in number of v

227 pontaneous atrial (p = 0.02) and ventricular arrhythmias (p = 0.03) in PVC-CM.

228 ld and/or moderate, and 24 +/- 7% for severe arrhythmia; p = 0.02).

229 We propose that respiratory sinus arrhythmia pacing reverse-remodels the heart in heart fa

230 For some drug-induced arrhythmias, particularly torsades de pointes, risk fact

231 iovascular complications were shock, cardiac arrhythmias, pericardial effusion, and coronary artery d

232 most widely used risk marker for ventricular arrhythmia potential and thus an important component of

233 This study determined ventricular arrhythmia prevalence, severity, phenotypical context, a

234 have only a moderate effect on prevention of arrhythmia progression.

235 m initial failure of the procedure or atrial arrhythmia recurrence after a 90-day blanking period to

236 Arrhythmia recurrence after AF ablation may represent a

237 erapy for atrial fibrillation (AF); however, arrhythmia recurrence and repeat procedures are common.

238 A connections at a first AF ablation reduces arrhythmia recurrence during follow-up.

239 to drug therapy for the prevention of atrial arrhythmia recurrence in patients with paroxysmal atrial

240 The overall arrhythmia recurrence rate between 3 and 12 months was 4

241 s both AM stage and WBZ were associated with arrhythmia recurrences anytime during follow-up.

242 f distal CS to LA connections reduced atrial arrhythmia recurrences compared with standard pulmonary

243 results and identify factors associated with arrhythmia recurrences in a cohort of patients with myoc

244 Abstinence from alcohol reduced arrhythmia recurrences in regular drinkers with atrial f

245 low-up of 170+/-22 days, there were 7 atrial arrhythmia recurrences in the standard group and 1 recur

246 among participants without documented atrial arrhythmia recurrences.

247 An increase in the incidence of arrhythmias related to inflammation such as atrial fibri

248 mdxS3E mice were protected against inducible arrhythmias, related lethality, and the development of c

249 quent cardiac edema to the genesis of atrial arrhythmias remains unknown.

250 lar arrhythmias, congestive heart failure or arrhythmias requiring admission to an intensive care uni

251 is unclear whether these differing types of arrhythmia result from direct and perhaps distinct effec

252 s, including clinically relevant ventricular arrhythmias, resuscitated cardiac arrest, acute kidney f

253 ars; 13 +/- 2%) was strongly associated with arrhythmia severity (8 years; 10 +/- 2% for no/trivial,

254 indings show that cardiac hMSCs can regulate arrhythmia substrates by remodeling their secretome in d

255 human MSCs (hMSCs) remodels and can regulate arrhythmia substrates.

256 IGF-1) the cardiac hMSC secretome can rescue arrhythmia substrates.

257 gest that suppression of RA directly reduces arrhythmia susceptibility and reinforces the concept tha

258 ed vascular leak can acutely increase atrial arrhythmia susceptibility by disrupting ID nanodomains a

259 daily changes in cardiac electrophysiology, arrhythmia susceptibility, and Ca(2+) handling have not

260 lity of this system to control RA and reduce arrhythmia susceptibility, in vivo.

261 We obtained surface ECGs and analyzed arrhythmia susceptibility; we observed prolonged QRS dur

262 Arrhythmia syndromes associated with KCNJ2 mutations hav

263 r patients with potentially life-threatening arrhythmia syndromes like long QT syndrome (LQTS).

264 -degree relatives, female relatives, primary arrhythmia syndromes, relatives with manifest inherited

265 pproach to treating life-threatening cardiac arrhythmia syndromes.

266 y injecting the designed channel current for arrhythmia termination in human atrial myocytes using dy

267 cause arrhythmias and knowledge of distinct arrhythmias that may be drug-induced are essential for c

268 ical system, typically caused by ventricular arrhythmias, that can lead to sudden cardiac death (SCD)

269 end points included freedom from symptomatic arrhythmia, the atrial fibrillation burden, and quality

270 However, little is known about these arrhythmias-their frequency, the underlying mechanisms,

271 complete recovery, persistent heart failure, arrhythmias, thromboembolic events, and death.

272 tractions and increased incidence of cardiac arrhythmias under stress conditions.

273 shock and concomitant refractory ventricular arrhythmia undergoing bailout ablation due to inability

274 Because cardiac arrhythmias underlie most cardiac arrests and increasing

275 Excess mortality was substantial for severe arrhythmia (univariate hazard ratio [HR]: 2.70; 95% conf

276 lure, chronic obstructive pulmonary disease, arrhythmia, urinary tract infection, septicemia, and str

277 e sudden cardiac arrest (SCA) or ventricular arrhythmia (VA).

278 %, p = 0.023), and more pre-LVAD ventricular arrhythmias (VA) (77% vs 60%, p = 0.048).

279 opathy (ARVC) is associated with ventricular arrhythmias (VA) and sudden cardiac death (SCD).

280 The association of the onset of ventricular arrhythmias (VA) with 0- to 21-day moving averages of PM

281 er-defibrillator utilization nor ventricular arrhythmia varied by sex.

282 Ventricular arrhythmias (VAs) have never been systematically investi

283 that may give rise to reentrant ventricular arrhythmias (VAs).

284 cell and tissue scales to expose fundamental arrhythmia vulnerability mechanisms and complex interact

285 Severe arrhythmia was also associated with higher rates of mort

286 A composite outcome of severe ventricular arrhythmia was assessed.

287 Presence of ventricular arrhythmia was associated with male sex, bileaflet prola

288 Ventricular arrhythmia was frequent (43% with at least ventricular e

289 Long-term severe arrhythmia was independently associated with notable exc

290 Severe ventricular arrhythmia was independently associated with presence of

291 After ablation and scar modification, the arrhythmia was noninducible in 19 patients (91%).

292 The follow-up period for all arrhythmias was from surgery until hospital discharge or

293 variability (time and frequency domain) and arrhythmias were compared by 24h-Holter, before, and 1 y

294 Clinically important arrhythmias were detected by Holter monitoring in 36 out

295 en stimulated with isoproterenol; the lethal arrhythmias were rescued, in part, by propranolol pre-tr

296 Furthermore, these arrhythmias were significantly decreased with propranolo

297 Arrhythmias were significantly increased among patients

298 al and an increased frequency of ventricular arrhythmias when used for treatment of COVID-19.

299 hm abnormalities (i.e. sinus pause and sinus arrhythmias) when compared to control mice.

300 osed that reinstatement of respiratory sinus arrhythmia would improve cardiac function in rats with h