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Carbamazepine
Published in Stanley R. Resor, Henn Kutt, The Medical Treatment of Epilepsy, 2020
CBZ may lead to mild cardiac conduction disturbances in approximately 20% of patients with epilepsy. In patients with previous cardiac disease, clinically relevant conduction problems leading to syncope and death may occur even at low plasma concentrations (82–85). Sinoatrial block has been described (86,87). On the positive side, users of CBZ showed less mortality due to ischemic heart disease than controls, possibly related to CBZ-induced higher concentrations of plasma high density lipoprotein (88).
Sitafloxacin
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Rhonda L. Stuart, Ashwin Swaminathan
Preclinical toxicological evaluation of fluoroquinolones in animals showed that they could induce cardiovascular effects such as hypotension or tachycardia after intravenous injection. In addition, quinolones have the potential to directly alter cardiac rhythm, prolong the QTc interval, and produce cardiac arrythmias. Fluoroquinolones prolong the QTc interval by blocking the cardiac voltage-gated potassium channels (Anderson et al., 2001; Falagas et al., 2007). In a phase II, open, multicenter, randomized study, sitafloxacin (400 mg daily) was administered to 35 patients. One patient was noted to have sinoatrial block on day three that was considered to be possibly related to the study drug (Feldman et al., 2001). In 84 subjects treated with high-dose sitafloxacin (400, 600, or 800 mg twice daily), there were no subjects whose QT interval was prolonged more than 60 msec (Anderson, 2008).
Clinical studies on Shengmai San
Published in Kam-Ming Ko, Shengmai San, 2002
Ye-Zhi Rong, Mei-Hua Zhao, Bao-Jing Lu, Xiang-Yang Zhu, Shang-Biao Lu, Ya-Chen Zhang, Jie Chen, Kam-Ming Ko
There is still some controversy about the diagnostic criteria for viral myocarditis. Under clinical conditions, there are no rapid and highly specific diagnostic means available for viral myocarditis. According to the National Forum on Myocarditis and Myocardial Diseases held in 1987 (Editorial 1987), the diagnostic criteria for viral myocarditis include: (1) clinical symptoms and signs (upper respiratory tract or digestive tract) of viral infection; (2) heart performance at the acute stage or within 1–3 weeks after viral infection, persistent and frequent pulses unrelated to feverish condition, edema, coughing, non-productive asthma, chest distress, heart malfunctions with unknown causes, and other signs such as cardiomegaly, cardiac murmur, the third and fourth heart sound and arrhythmia; and (3) various arrhythmias found in the electrocardiogram: (a) atrioventricular block or sinoatrial block, bundle branch block, (b) more than two channels with its ST segment being lowered or elevated, or abnormal Q concentration, (c) frequent, multiform, polyfocal or paired/parallel premature beat, burst or paroxysmal supraventricular tachycardia and ventricular tachycardia, beating and fibrillation, (d) frequent atrial or ventricular premature beat, (e) inverted T-wave (either bipolar or flattened). In addition, other indications of viral myocarditis include positive response of PCR EVS-RNA test and a four-fold increase in antibodies against Coxsackie B virus (Zhao et al. 1996), positive response of serum creatine phosphokinase (CK) and its isozyme (CK-MB), and positive response of serum myocardial troponin T (cTnT) and troponin I (cTnI). With regard to sensitivity and specificity, serum cTnI is superior to cTnT as a diagnostic for acute viral myocarditis. In addition, cTnI also provides a wider time window for diagnosis. Hence, serum cTnI is a highly recommended diagnostic marker for viral myocarditis in clinical situations. Finally, the diagnosis of viral myocarditis should be carefully distinguished from other pathological conditions, such as hyperthyroidism, β-adrenoreceptors hyperfunction syndrome, coronary heart disease, rheumatic myocarditis, toxic myocarditis, and primary/secondary cardiomyopathy, that can also affect the myocardium.
Reviewing the evidence surrounding preservative-free tafluprost/timolol fixed-dose combination therapy in open-angle glaucoma and ocular hypertension management: a focus on efficacy, safety, and tolerability
Published in Expert Opinion on Drug Safety, 2022
The addition of timolol has been shown to enhance the tolerability of PGA agents in FC therapies [35]. Timolol is associated with few topical side effects, although it has some important systemic adverse effects on the cardiac and respiratory systems [40,41,59,60]. It is associated with symptomatic bradycardia and bronchospasms [40,41,59,60]. Timolol-containing FC glaucoma medications are therefore contraindicated in people with sinus bradycardia, sick sinus syndrome, including sinoatrial block, second- or third-degree atrioventricular block not controlled with pacemaker, overt cardiac failure, and cardiogenic shock [1]. People with reactive airway disease, including current bronchial asthma, history of bronchial asthma, or severe chronic obstructive pulmonary disease, should not be prescribed a timolol-containing therapy [1]. Individuals with cardiac disorders (e.g. coronary heart disease and cardiac failure) and hypotension should be critically assessed and monitored for deterioration or adverse events (AEs) when treated with timolol-containing therapies/regimens [1]. In addition, beta-blockers such as timolol may mask the signs and symptoms of acute hypoglycemia and should be used with caution in individuals with labile diabetes [1]. Tafluprost and other PGAs may be associated with peri-orbitopathy, including eyelash growth, darkening of the eyelid skin, and increased iris pigmentation [1]. Some of these changes may be permanent and can lead to differences in appearance between the eyes when only one eye is treated [1].
Long-term effect of catheter ablation on tachycardia-bradycardia syndrome: evidenced by 10 years follow up
Published in Acta Cardiologica, 2020
Shushan Zhang, Yanzong Yang, Yunlong Xia, Lianjun Gao, Xuanhe Zhang, Gary Tse, Xiaomeng Yin, Shiyu Dai, Dong Chang
Around 40–70% of atrial tachyarrhythmia are associated with sinus node dysfunction (SND) [8]. The latter comprises abnormalities, including sinus arrest, sinus bradycardia, sinoatrial block, and alternating episodes of tachycardia and bradycardia. The main feature of classical SND is sinus bradycardia and sinus arrest, in the presence or absence of atrial tachycardia. TBS is characterised by paroxysmal AF, atrial flutter (AFL), or atrial tachycardia (AT), with sinus bradycardia/junctional escape rhythm or arrest secondary to these tachyarrhythmia. Many mechanisms of TBS have been put forward. Firstly, rapid ventricular rate leading to the insufficiency of the sinus arterial supply [9], which reduces the automaticity function of the sinoatrial node (SN). Secondly, atrial tachyarrhythmia can induce the release and accumulation of acetylcholine in the atrial myocardium, thereby promoting K+ efflux and negative spontaneous depolarisation [10]. Therefore, it decreases the amplitude of spontaneous depolarisation and eventually reduces the automaticity of SN. Thirdly, TBS is also related to higher vagal activity in the context of AF [11], which can cause sinus node dysfunction. Finally, atrial tachycardia could decrease the expression of HCN4 mRNA and funny current (If), thereby resulting in electrophysiological remodelling and SND [12,13]. The above factors might account for the long pauses and bradycardia in TBS.
Swallow presyncope in an athletic patient caused by third-degree atrioventricular block
Published in Acta Clinica Belgica, 2018
Axel Van Damme, Tine De Backer, Philippe Vanderheeren
In emergency departments, syncope is a frequent and potential life threatening reason for referral with 1.21–1.5% of the admissions being accounted to syncope [1,2] Swallow syncope is a neurally mediated syncope. Current hypothesis states that it is caused by an exceeding vagotonic reflex following oesophageal dilatation which in turn leads to cerebral hypoperfusion. Arrhythmias on their turn are rare causes of swallow syncope. Reported cases include sinus bradycardia, sinoatrial block, and complete atrial and ventricular asystole and atrioventricular block [3–7]. The ESC guidelines state that patients with ‘recurrent, unpredictable reflex syncopes and documented AV block’ have a class IIa recommendation for pacemaker implantation (evidence C) [8].