Incidence Of Supraventricular Tachyarrhythmias Research Articles

Atrial approaches in mitral valve surgery: a propensity analysis of differences in the incidence of clinically relevant adverse effects

BackgroundThe lack of evidence on complications using mitral valve approaches leaves the choice of risk exposure to the surgeon’s preference, based on individual experience, speed, ease, and quality of exposure.MethodsThe present study analysed patients undergoing mitral valve surgery using a superior transseptal approach or a left-atrial approach between 2006 and 2018. We included first-time elective mitral valve procedures, isolated, or combined, without a history of rhythm disturbances. We used propensity score matching based on 26 perioperative variables. The primary endpoint was the association between the superior transeptal approach and clinically significant adverse outcomes, including arrhythmias, need for a permanent pacemaker, cerebrovascular events, and mortality.ResultsA total of 652 patients met the inclusion criteria; 391 received the left atrial approach, and 261 received the superior transseptal approach. After matching, 96 patients were compared with 69 patients, respectively. The distribution of the preoperative and perioperative variables was similar. There was no difference in the incidence of supraventricular tachyarrhythmias or the need for treatment. The incidence of nodal rhythm (p = 0.008) and length of stay in intensive care (p = 0.04) were higher in the superior transseptal group, but the need for permanent pacemaker implantation was the same. Likewise, there was no difference in the need for anticoagulation due to arrhythmia, the incidence of cerebrovascular events or mortality in the postoperative period or in the long-term follow-up.ConclusionWe did not find an association with permanent heart rhythm disorders or any other significant adverse clinical outcome. Therefore, the superior transeptal approach is useful and safe for mitral valve exposure.

Risk Model to Predict Supraventricular Arrhythmias in Multiple Myeloma Patients Undergoing Autologous Stem Cell Transplant

Multiple Myeloma (MM) are often treated with high-dose melphalan and autologous stem cell transplant (ASCT). Cardiac toxicity, including Supraventricular tachyarrhythmias (SVT), is a fairly common complication which may be related to Melphalan, the transplanted stem cells or effects of para-proteinemia on the conduction system. Here, we sought to determine the incidence of SVT and its predisposing factors in this setting. Methods We reviewed the 100-day post-ASCT clinical course of all MM patients treated from 2007 to 2017 that had undergone ASCT at our institution. Clinical data, EKG and Echocardiography data were extracted. QRS amplitude was measured in the V2 precordial lead as the distance from the R peak to S peak. Both atrial fibrillation and atrial flutter were classified as SVT. Results A total of 222 patients were included in the study population. Amifostine was used before all ASCT to reduced oral mucositis. Patient median age was 60.6 (range: 36-79), 110 patients (49%) were male and the 112 female (51%). Median pre-ASCT QRS amplitude was 1.7 millivolt (mV) (range: 0.3-4.4). Median QRS duration was 90 millisecond (mS, range: 60-208). Only 166 patients received a pre-ASCT ECHO. Median time of pre-ASCT and post-ASCT ECHO were 38 days (range: 1-333 days) and 55 days (range: 4-118), respectively. Seventeen patients (8%) developed SVT during or after ASCT with a median time of 12 days post-ASCT (range: 1-97 days). Median time of the length of hospital stay between patients without SVT and with SVT was different, 15 vs. 19 days (p-value Conclusion Taken together, our results suggest that SVT represents an important cause of morbidity and is associated with longer hospital stay for MM patients undergoing ASCT. The presence of abnormal renal function, LVSD, or hypertension at baseline identifies patients at greater risk of developing SVT following ASCT.

Factors Influencing Incidence of Supraventricular Arrhythmias during and after Autologous Stem Cell Transplant in Multiple Myeloma

Multiple Myeloma (MM) are often treated with high-dose melphalan and autologous stem cell transplant (ASCT), followed by maintenance therapy (McCarthy et al. JCO, 2017). Cardiac toxicity is a potentially serious complication and is a dose limiting toxicity of high-dose melphalan. Furthermore, the overall risk of cardiac event is higher in MM patients compared to age- and gender-matched individuals without MM (Kistler et al. Clin Lymph, Myel & Leuk, 2016). Pre-transplant cardiac screening may help prevent major cardiac complications such as severe heart failure, cardiac tamponade, or life-threatening cardiac arrhythmias. Supraventricular tachy arrhythmias (SVT) are a common complication which may be related to Melphalan, the transplanted stem cells or effects of para-proteinemia on the conduction system. Here, we sought to determine the incidence of SVT and its predisposing factors in this setting.Methods: We reviewed the 100-day post-ASCT clinical course of all MM patients treated from 2007 to 2017 that had undergone ASCT at University Hospitals Cleveland Medical Center. Patients also diagnosed with cardiac Light Chain Amyloidosis (AL) were excluded. Clinical data on the following characteristics were collected: patients' demographics, disease characteristics, pre-ASCT comorbidities and cardiovascular-related medication use, electrocardiography (ECG) and echocardiography (ECHO). ECG and ECHO studies was limited to one year prior to ASCT. Presence of left ventricle hypertrophy (LVH), ejection fraction (EF), impaired relaxation or abnormally low QRS voltage on pre-ASCT were recorded. QRS amplitude was measured in the V2 precordial lead as the distance from the R peak to S peak. Both atrial fibrillation and atrial flutter were classified as SVT. Continuous variables were compared using the unpaired t-test, and categorical variables were compared using the two-tailed Fisher's exact test. A multiple logistic regression model was fit to a model containing all the collected potential risk factors. Odds ratios (ORs) and confidence intervals (CIs) were estimated from the estimated betas in the model. A two-tailed p value < 0.05 was considered to be statistically significant.Results: A total of 222 patients were included in the study population. Amifostine was used before all ASCT to reduced oral mucositis. Patient median age was 60.6 (range: 36-79), 110 patients (49%) were male and the 112 female (51%). Median pre-ASCT QRS amplitude was 1.7 millivolt (mV) (range: 0.3-4.4). Median QRS duration was 90 millisecond (mS, range: 60-208). Only 166 patients received a pre-ASCT ECHO. Median time of pre-ASCT and post-ASCT ECHO were 38 days (range: 1-333 days) and 55 days (range: 4-118), respectively. Seventeen patients (8%) developed SVT during or after ASCT with a median time of 12 days post-ASCT (range: 1-97 days). Median time of the length of hospital stay between patients without SVT and with SVT was different, 15 vs. 19 days (p-value < 0.001). There was no statistically significant between average melphalan dose utilized as the conditioning regimen, infused CD34 dosage, transplant-associated weight loss, time from diagnosis or length of pre-ASCT exposure to proteasome inhibitors between two cohorts (Table-1 and 2). Also, there was no association between pre-ASCT use of anti-lipid lowering agents, beta-blockers, angiotensin-converting enzyme inhibitor or angiotensin receptor inhibitors. Out of all pre-ASCT comorbidities renal insufficiency (9% vs. 41%, p-value: 0.017) and HTN (49% vs. 76%, p-value: 0.045) were predictor, of SVT occurrence in the univariate analysis. Multivariate analysis indicated that renal insufficiency at baseline (OR: 3.6, 95% CI: 2.1-4.8, p-value < 0.001), left ventricular systolic dysfunction (LVSD, OR: 3.0, CI: 1.1-5.1, p-value: 0.003), and hypertension (OR: 2.5, CI: 1.2-4.6, p-value: 0.028), were significantly associated with the development of SVT after ASCT (Fig. 1).Conclusion: Taken together, our results suggest that SVT represents an important cause of morbidity and is associated with longer hospital stay for MM patients undergoing ASCT. The presence of abnormal renal function, LVSD, or hypertension at baseline identifies patients at greater risk of developing SVT following ASCT. Further studies are warranted to establish robust risk models that may predict SVT in MM patients prior to and during ASCT. DisclosuresCaimi:ADC Therapeutics: Research Funding; Celgene: Speakers Bureau; Kite Pharma: Membership on an entity's Board of Directors or advisory committees; Genentech: Membership on an entity's Board of Directors or advisory committees. Malek:Takeda: Consultancy, Speakers Bureau; Amgen: Consultancy, Speakers Bureau; Sanofi: Consultancy, Speakers Bureau; Celgene: Consultancy, Speakers Bureau; Janssen: Consultancy, Speakers Bureau.

Impaired tissue clearance of verapamil in rat cardiac hypertrophy results in transcriptional repression of ion channels

Heart hypertrophy is a common cardiac complication of sustained arterial hypertension and is accompanied by an increased incidence of supraventricular tachyarrhythmia, such as atrial fibrillation and atrial flutter. Verapamil, a phenyalkylamine, belongs to the group of calcium channel antagonists (class IV antiarrhythmic drugs) and is frequently used for the management of supraventricular tachycardia and for ventricular rate control in atrial fibrillation and atrial flutter.Verapamil heart tissue and plasma levels after intraperitoneal dosing of spontaneously hypertensive and normotensive rats were investigated. Transcript expression of various ion channels, ion transporters, calcium handling, and cytoskeletal proteins by reverse transcriptase-polymerase chain reaction (RT-PCR) were further investigated. There was no difference in plasma pharmacokinetics when hypertensive and normotensive animals were compared. Strikingly, the tissue clearance of verapamil was highly significantly impaired in heart tissue of hypertensive animals. Gene expression analysis showed the repression of many cardiac-specific genes in spontaneously hypertensive but not in normotensive rats, therefore providing evidence for different modes of action in healthy and hypertrophic hearts.Verapamil heart tissue levels differed dramatically between normotensive and hypertensive rats and resulted in repression of many cardiac ion channels, ion transporters, and calcium handling proteins. A disturbed ion homeostasis induced by critical tissue levels of verapamil is therefore proposed as a molecular rational for its pro-arrhythmogenic activity. The observed changes can be a significant determinant of spatial electrophysiological heterogeneity, thereby contributing to increased conductance disturbance as observed with some patients.

Supraventricular tachyarrhythmia as a cause of sudden cardiac arrest

Supraventricular tachyarrhythmias (SVTA) are an accepted cause of cardiac arrest in patients with Wolff-Parkinson-White syndrome (WPW) and hypertrophic cardiomyopathy but their participation in other conditions is less well understood. The purpose of the study was to examine the role of SVTA in sudden cardiac arrest (SCA) by comprehensive evaluation of patients successfully resuscitated from SCA. A total of 169 survivors of SCA in the absence of acute myocardial infarction underwent systematic evaluation that included echocardiography, Holter monitoring, coronary angiography and electrophysiological study (EPS) with additional testing in selected cases using provocative drug testing with isoproterenol, ajmaline or ergonovine. SVTA was found as the only possible cause or as the cause facilitating SCA in 29 patients: (1) 3 had a WPW syndrome related to accessory pathway with short refractory period; (2) for 12 patients, SVTA was the cause of cardiovascular collapse; heart disease (HD) was present in 11 cases, but disappeared in two of four with dilated cardiomyopathy after the restoration of sinus rhythm; (3) in 14 patients, SVTA degenerated either in a VF or ventricular tachycardia (VT); HD was present in 12 cases, but disappeared in one; two had no HD and recurrent similar arrhythmia was documented by cardiac defibrillator in one of them. SVTA induced coronary ischemia was the main cause of SCA. Rapid SVTA was a cause of SCA, either by cardiovascular collapse or by the degeneration in VT or VF. The complication generally occurred in patients with advanced HD or with rapid SVTA-induced cardiomyopathy and rarely in patients without HD. The incidence of SVTA as the only cause or the facilitating cause of SCAs is probably underestimated, because it is difficult to prove.

Supraventricular tachyarrhythmia as early indicator of a complicated course after esophagectomy

In a group of 89 consecutive patients with a standardized operative procedure, the incidence of supraventricular tachyarrhythmia (SVT), predisposing risk factors (preoperative and intraoperative factors and parameters of intensive care strategy) and therapeutic strategies were evaluated. Operative treatment consisted of transthoracic esophagectomy, gastric interposition and intrathoracic anastomosis. Overall hospital mortality was 6.7%. In 32 (37%) patients a new onset SVT occurred. Age and elevated body temperature were the only significant risk factor for SVT in the multivariate analysis, their odds ratios being 1.3 for each year above 58 and 5.6 for each degree above 37.8 degrees C, respectively. Secondary risk factors were history of hypertension and use of epinephrine, the corresponding odds ratios being 6.6 and 10.2. Digitalis (2/32) and calcium-antagonists (2/9) were unsatisfactory, while beta-blockers (13/20) and amiodarone (12/12) were efficient therapeutic agents. Incidence of SVT was significantly correlated with the development of postoperative septic complications.

Proposed Diagnostic Criteria for the Brugada Syndrome

Asyndrome characterized by ST-segment elevation in right precordial leads (V1 to V3) that is unrelated to ischemia, electrolyte disturbances, or obvious structural heart disease was reported as early as 1953,1 but was first described as a distinct clinical entity associated with a high risk of sudden cardiac death in 1992.2–4⇓⇓ The Brugada syndrome is a familial disease that displays an autosomal dominant mode of transmission, with incomplete penetrance and an incidence ranging between 5 and 66 per 10 000. In regions of Southeast Asia where it is endemic, the clinical presentation of Brugada syndrome is distinguished by a male predominance (8:1 ratio of male:female) and the appearance of arrhythmic events at an average age of 40 years (range: 1 to 77 years).2,5⇓ Although a number of candidate genes are considered plausible, thus far the syndrome has been linked only to mutations in SCN5A , the gene encoding for the α subunit of the sodium channel.6 A number of ambiguities exist concerning the diagnosis of Brugada syndrome. The electrocardiographic signature of the syndrome is dynamic and often concealed, but can be unmasked by potent sodium channel blockers such as flecainide, ajmaline, and procainamide,7 although the specificity of this effect for uncovering patients at risk for sudden death has been an issue of concern. A recent report by Remme et al8 has shown that the number of idiopathic ventricular fibrillation patients diagnosed as having Brugada syndrome is a sensitive function of the diagnostic criteria applied. What are the proper diagnostic criteria for identifying Brugada syndrome? A definitive answer to this question has been out of reach and is the reason for the establishment of a special Arrhythmia Working Group of the European Society of Cardiology that met from August 31 to …

Frequency of supraventricular tachyarrhythmias in arrhythmogenic right ventricular dysplasia

The incidence of supraventricular tachyarrhythmias in patients with arrhythmogenic right ventricular dysplasia (ARVD) is unknown. 1–5 We report on 72 consecutive patients with the diagnosis of ARVD studied at Jean Rostand Hospital.

Metoprolol in acute myocardial infarction (MIAMI). A randomised placebo-controlled international trial

The effect of metoprolol on mortality and morbidity after 15 days, was compared with that of placebo in a double-blind randomised international trial (the MIAMI trial) in patients with definite or suspected acute myocardial infarction (AMI). Treatment with intravenous metoprolol (15mg) or placebo was started shortly after the patient's arrival in hospital within 24 h of the onset of symptoms, and then oral treatment (200 mg daily) was continued for the study period (15 days). Of the 5778 patients included, 2901 were allocated to placebo and 2877 to metoprolol. Definite AMI was confirmed in 4127 patients. There were 142 deaths in the placebo group (4.9%) and 123 deaths in the metoprolol group (4.3%), a difference of 13 per cent with 95 per cent confidence limits of −8 to +33 per cent, not statistically significant (P=0.29). Previously recorded risk indicators of mortality were analysed in retrospect. These indicated that there was a category which showed higher risk which contained approximately 30% of all randomized patients. In these, the mortality rate in the metoprolol treated group was 29% less than in the placebo group. In the remaining lower risk categories there was no difference between the treatment groups. This subset analysis must be interpreted with caution in view of the findings from other similar studies. Positive effects were observed on the incidence of definite AMI and on serum enzyme activity in patients treated early ( <7h). There was no significant effect on ventricular fibrillation but the number of episodes tended to be lower in the metoprolol treated patients during the later phase (6–15 days; 24 vs 54 episodes). The incidence of supraventricular tachyarrhythmias, the use of cardiac glycosides and other antiarrhythmics, and the need for pain-relieving treatment were significantly diminished by metoprolol amongst all randomised patients. Adverse events associated with metoprolol were infrequent, expected, and relatively mild.

Influence of propranolol on supraventricular tachycardia early after coronary artery revascularization: A randomized trial

A total of 116 patients undergoing coronary revascularization were randomized preoperatively in a double-blind manner to receive 80 mg daily of propranolol or placebo in the postoperative period. Preoperatively, all patients had been receiving at least 80 mg of propranolol a day to the time of the operation. In addition, all patients had a left ventricular ejection fraction of 0.4 or more, no history of supraventricular tachyarrhythmia (SVT), and no need of digitalis preparations or other antiarrhythmic drugs. All patients were monitored for 5 days and propranolol or placebo was started 24 hours postoperatively. SVT was documented with biatrial electrograms in all cases. Study groups were similar in postoperative creatine kinase MB levels and postoperative weight gain, but the placebo group tended to be older and have more grafts per patient. Seven patients randomized were dropped from the study, two with perioperative infarction, four with persistent ventricular arrhythmias necessitating quinidine or procainamide, and one with persistent postoperative hypotension (placebo). There were no significant differences in the incidence of postoperative SVT in these two groups: 13.2% in the propranolol group and 16.1% in the placebo group. We conclude that 80 mg daily of propranolol given postoperatively to patients undergoing coronary revascularization does not effectively reduce the incidence of SVT.

Prevention of supraventricular tachyarrhythmia with low-dose propranolol after coronary bypass

Eighty-five patients receiving long-term propranolol therapy were randomized after aorta-coronary bypass grafting either to receive minidose propranolol (Group I) or to serve as controls (Group II). They were compared with 18 patients (Group III) who did not receive beta blocking agents prior to operation but were given propranolol postoperatively. Poor-risk patients (those having left ventricular aneurysms, low ejection fraction, or congestive heart failure) as well as patients who required catecholamines postoperatively were included in the study. All three groups were comparable with respect to all risk factors. Propranolol (5 to 10 mg/6 hr) was started through a nasogastric tube 6 hours after operation and continued orally in all patients in Groups I and III. Supraventricular tachyarrhythmia appeared in two of 37 patients in Group I (5%), 19 of 48 patients in Group II (40%), and five of 18 patients in Group III (27%). The incidence of supraventricular tachyarrhythmia was significantly lower in Group I than in Groups II and III (p less than 0.001, Group I versus Group II; p less than 0.01, Group I versus Group III). In conclusion, low-dose propranolol is very effective in preventing supraventricular tachyarrhythmia following aorta-coronary bypass in patients receiving beta blockers preoperatively. The increased tendency for postoperative supraventricular tachyarrhythmia to develop in these patients is attributed to hypersensitivity to adrenergic stimulation after propranolol withdrawal. The tachyarrhythmia can be prevented by early reinstitution of propranolol in low doses after the operation.

Immediate postoperative digitalization in the prophylaxis of supraventricular arrhythmias following coronary artery bypass

Regimens of acute preoperative digitalization have been evaluated previously in the prophylaxis of supraventricular tachycardias (SVT) following coronary artery bypass operations, with equivocal results. This study assesses the effectiveness of immediate postoperative digitalization on the incidence of arrhythmias in 407 consecutive patients recovering from myocardial revascularization. In 137 patients treated by our regimen, which begins digitalization within 4 hours postoperatively, the incidence of supraventricular tachyarrhythmias was 2%, while the corresponding figure for 270 untreated patients was 15%. Digitalization reduced the incidence of supraventricular arrhythmias significantly (p less than 0.01), whereas death, ventricular ectopy, and infarction rates were similar in the two groups. The few patients who did have supraventricular arrhythmias while receiving prophylactic digoxin were no more easily treated than patients in the undigitalized group. The timing of administration of digoxin for SVT prophylaxis may be more important than previously recognized. Immediately postoperative digitalization, theoretically preferable to preoperative regimens, is a safe, effective way to reduce the incidence of supraventricular arrhythmias following myocardial revascularization.

Supraventricular tachyarrhythmias after myocardial revascularization: A randomized trial of prophylactic digitalization

The success of prophylactic digitalization in reducing the incidence of supraventricular tachyarrhythmias (SVT) was studied in 140 randomly grouped, consecutive patients undergoing myocardial revascularization operations. The test group received either 1 or 1.5 mg. of digoxin the day before operation and were maintained postoperatively on 0.25 mg. of digoxin daily. There was a significant increase (p less than 0.05) in the incidence of SVT in the treated patients (17 of 61 or 27.8 percent) vs. the untreated patients (nine of 79 or 11.4 percent). There was no significant difference in SVT with the two digitalization dosage levels (31.6 percent with 1 mg. vs. 21.7 percent with 1.5 mg.). Prophylactic digitalization demonstrates no benefit in the prevention of SVT following myocardial revascularization and may, in fact, predispose the patient to these arrhythmias.