Permanent-temporary pacemakers in the management of patients with conduction abnormalities after transcatheter aortic valve replacement

Background

Damage to the cardiac conduction system requiring permanent pacemaker (PPM) implantation is a known adverse outcome of transcatheter aortic valve replacement (TAVR). A permanent-temporary pacemaker (PTPM) is a device that involves an active-fixation lead attached to an external pulse generator taped to the skin. We reviewed the utility of PTPMs as a temporary bridge measure after TAVR in patients with conduction abnormalities that do not meet conventional criteria for PPM placement.

Methods

Between January 01, 2013 and December 31, 2015, we analyzed 67 patients who received PTPM after TAVR. Baseline demographics, comorbidities, type and size of the valve, pre-TAVR electrocardiograms (ECGs), post-TAVR ECGs at 1 day, 1 month, and 6 months, and pacemaker interrogation results were reviewed for each patient if available.

Results

The mean age of patients was 80.5?±?9.1 years. PTPM were placed for 2.3?±?2.4 days. Among these patients, 44.8% (n?=?30) received a PPM prior to discharge. Male gender (OR 2.84, 95% CI 1.05–7.69, p?=?0.05) and an increase in QRS duration post-TAVR (p?=?0.01) were associated with PPM placement. Pacemaker interrogation data of 11 patients with PPM revealed that 27% (n?=?3) had <?1% V-pacing requirements and <?10% A-pacing requirements.

Conclusions

In post-TAVR patients who develop conduction abnormalities that do not meet conventional PPM implantation indications, PTPM safely provides a time period for further assessment and may prevent unnecessary PPM implantation. Male gender and an increase in QRS duration post-TAVR are associated with PPM implantation. Additionally, some patients may recover from their conduction disturbances and demonstrate low pacemaker utilization.

     

The role of angiotensin converting enzyme genotype in coronary artery ectasia

Coronary artery ectasia (CAE) is characterised by irregular, diffuse, saccular, or fusiform dilatation of the coronary arteries. Although the underlying mechanisms are not fully understood, CAE is considered to be an original form of vascular remodelling in response to atherosclerosis. However, it is not clear why some patients develop CAE while most do not. Experimental data suggest that activation of the renin angiotensin system may lead to an increased inflammatory response in the vessel wall or to an activation of matrix metalloproteinases. In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone and the development of aneurysms. Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE. We retrospectively evaluated 112 patients who underwent coronary angiography. ACE ID genotype was determined in two groups of patients. Group 1 consisted of 56 patients who were found to have CAE. Group 2 consisted of 56 patients with significant coronary artery disease (CAD) (> 50% stenosis in any of the major epicardial coronary arteries or their branches) but without any evidence of coronary ectasia. Polymerase Chain Reaction (PCR) was used to detect ACE genotype. The ratio of DD genotype was found to be greater in group 1 than group in 2 (39% versus 18%, respectively, P < 0.05). When assessed according to the presence of the I allele, it was greater was greater in group 2 than in group 1 (82.1% versus 60.7%, respectively, P < 0.05). The results indicate that an ACE DD genotype may be a risk factor for CAE.     

Increased Prevalence of Myocardial Injury in Patients with SARS-CoV-2 Viremia

BackgroundPatients with coronavirus disease 2019 (COVID-19) have a high prevalence of detectable troponin and myocardial injury. In addition, a subset of patients with COVID-19 has detectable severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral loads. The objective of this study was to understand the relationship among SARS-CoV-2 viremia, detectable troponin, and myocardial injury in hospitalized patients with COVID-19.MethodsSARS-CoV-2 plasma viral load was measured in plasma samples drawn from patients hospitalized for COVID-19 at 2 academic medical centers. Baseline characteristics and clinically obtained high-sensitivity cardiac troponin T (hs-cTnT) values were abstracted from the medical record. The main outcome was detectable hs-cTnT (≥6 ng/mL) and myocardial injury (hs-cTnT ≥14 ng/mL; >99th percentile for assay).ResultsA total of 70 hospitalized patients with COVID-19 were included in this study, with 39% females and median age 58 ± 17 years; 21 patients (30%) were found to have detectable SARS-CoV-2 viral load and were classified in the viremia group. Patients with viremia were significantly older than those without viremia. All of the patients with viremia (100%) had detectable troponin during hospitalization compared with 59% of patients without viremia (P = 0.0003). Myocardial injury was seen in 76% of patients with viremia and 38% of those patients without viremia (P = 0.004).ConclusionsHospitalized patients with COVID-19 with SARS-CoV-2 viremia have a significantly higher prevalence of detectable troponin and myocardial injury during their hospitalization compared with patients who did not. This first report of the relationship among SARS-CoV-2 viremia, detectable troponin, and myocardial injury in patients with COVID-19 points to additional mechanistic pathways that require deeper study to understand the complex interplay among these unique findings, cardiovascular outcomes, and mortality in COVID-19.     

Physical Frailty Phenotype and the Development of Geriatric Syndromes in Older Adults with Coronary Heart Disease

BackgroundFrailty, a clinical state of vulnerability, is associated with subsequent adverse geriatric syndromes in the general population. We examined the long-term impact of frailty on geriatric outcomes among older patients with coronary heart disease.MethodsWe used the National Health and Aging Trends Study, a prospective cohort study linked to a Medicare sample. Coronary heart disease was identified by self-report or International Classification of Diseases (ICD) codes 1-year prior to the baseline visit. Frailty was measured using the Fried physical frailty phenotype. Geriatric outcomes were assessed annually during a 6-year follow-up.ResultsOf the 4656 participants, 1213 (26%) had a history of coronary heart disease 1-year prior to their baseline visit. Compared to those without frailty, subjects with frailty were older (ages ≥75: 80.9% vs 68.9%, P < 0.001), more likely to be female, and belong to an ethnic minority. The prevalence of hypertension, stroke, falls, disability, anxiety/depression, and multimorbidity were much higher in the frail, than nonfrail, participants. In a discrete time survival model, the incidence of geriatric syndromes during 6-year follow-up including 1) dementia, 2) loss of independence, 3) activities of daily living disability, 4) instrumental activities of daily living disability, and 5) mobility disability were significantly higher in the frail than in the nonfrail older patients with coronary heart disease.ConclusionIn patients with coronary heart disease, frailty is a risk factor for the accelerated development of geriatric outcomes. Efforts to identify frailty in the context of coronary heart disease are needed, as well as interventions to limit or reverse frailty status for older patients with coronary heart disease.     

The mitotic kinesin CENP-E is a processive transport motor

In vivo studies suggest that centromeric protein E (CENP-E), a kinesin-7 family member, plays a key role in the movement of chromosomes toward the metaphase plate during mitosis. How CENP-E accomplishes this crucial task, however, is not clear. Here we present single-molecule measurements of CENP-E that demonstrate that this motor moves processively toward the plus end of microtubules, with an average run length of 2.6 +/- 0.2 mum, in a hand-over-hand fashion, taking 8-nm steps with a stall force of 6 +/- 0.1 pN. The ATP dependence of motor velocity obeys Michaelis-Menten kinetics with K(M,ATP) = 35 +/- 5 muM. All of these features are remarkably similar to those for kinesin-1-a highly processive transport motor. We, therefore, propose that CENP-E transports chromosomes in a manner analogous to how kinesin-1 transports cytoplasmic vesicles.     

Optimization of cardiac resynchronization therapy after implantation

Many patients do not respond clinically to cardiac resynchronization therapy (CRT), despite clinical and survival benefits demonstrated in numerous clinical trials. This has led to focused evaluation from preimplant issues, as to who is an appropriate candidate for CRT, to postimplant issues, more specifically, optimizing device programming in CRT. CRT studies have used simultaneous biventricular pacing, but with advancing echocardiographic technology, the role of dyssynchrony, or mechanical delay in contraction of the ventricles, suggests that individually tailoring ventricular pacing improves hemodynamics. Atrial to ventricular timing affects left ventricular filling and cardiac output, whereas the right to left ventricular pacing delay also improves systolic and diastolic performance. The importance of device programming parameters and optimal pacing delays in biventricular pacing is reviewed in this article.     

Change in the retrograde atrial activation sequence following radiofrequency modification of the atrioventricular node: implications for the electrophysiologic circuit of a variant of atrioventricular nodal reentrant tachycardia

INTRODUCTION: Despite the great success in treating AV nodal reentrant tachycardia (AVNRT) with radiofrequency modification of the AV node, the dimensions of the electrophysiologic circuit of this arrhythmia remain unclear, and simple models fail to explain all tachycardia-related phenomena. METHODS AND RESULTS: We describe three unusual cases of supraventricular tachycardia (SVT). In all three cases, retrograde atrial activation during ventricular pacing or during SVT manifested local left atrial electrograms recorded from the coronary sinus preceding the septal atrial electrograms (eccentric activation), with earliest atrial activity at the lateral or posterolateral mitral annulus. Electrophysiologic maneuvers and observations were consistent with AVNRT as the mechanism in each case. In all cases, radiofrequency modification of the AV node eliminated inducible SVT and abolished dual pathway AV nodal physiology. The retrograde atrial activation sequence during ventricular pacing changed after ablation in each case, with septal atrial electrograms preceding left atrial electrograms recorded from the coronary sinus (concentric activation). CONCLUSION: The observations in these cases cannot be explained by the traditional model of slow, fast, and intermediate AV nodal pathways. A model incorporating a circuit close to the AV node with left atrial and coronary sinus connections is proposed.     

May maternal anti-mullerian hormone levels predict adverse maternal and perinatal outcomes in preeclampsia?

Background: Prediction of preeclampsia and adverse maternal and perinatal outcomes with biomarkers has been proposed previously. Anti-mullerian hormone (AMH) is a growth factor, which is primarily responsible of the regression of the mullerian duct, but also used to predict ovarian reserve and decreases with age similar to the fertility.

Aim: To evaluate the predictive role of maternal anti-mullerian hormone (mAMH) in adverse maternal and perinatal outcomes in preeclampsia.

Methods: This prospective case-control study was conducted at current high-risk pregnancy department in a tertiary research hospital and 45 cases with preeclampsia classified as study group and 42 as control group. Data collected and evaluated were; age, body mass index (BMI), marriage duration (MD), gestational weeks (GW), gravidity, parity, mode of delivery, birth weight, newborn Apgar score, newborn gender, maternal complication, perinatal outcome, some laboratory parameters and mAMH. The association between mAMH levels and maternal and fetal outcomes were evaluated.

Results: There were no statistically significant differences between groups in terms of age, BMI, MD, gravidity, parity and newborn gender (p?>?0.05). GW, vaginal delivery, birth weight, newborn Apgar score, were statistically significantly lower in preeclamptic patients when compared with non-preeclamptic patients (p?<?0.001). Adverse maternal and perinatal outcomes were statistically significantly higher in the study group (p?<?0.001). The laboratory values [alanine transaminase (ALT), aspartate transaminase (AST), blood urea nitrogen (BUN), creatinine, lactic dehydrogenase (LDH), uric acid and fibrinogen) were statistically significantly lower in the control group (p?<?0.001). The mAMH level was significantly lower in the preeclamptic group (p: 0.035). There was no correlation between mAMH levels and demographic and clinical parameters. The area under the ROC curve (AUC) was 0.590 and the cut-off value was 0.365?ng/ml with sensitivity of 67.4% and specificity of 47.1% for mAMH. Logistic regression analysis showed a statistically insignificance between mAMH and maternal complication and perinatal outcome (p: 0.149).

Conclusion: According to this study, mAMH level was lower in preeclamptic patients than in normal pregnants, and is found to be a discriminative factor with low sensitivity and specificity. There was no relationship between mAMH and adverse maternal and perinatal outcomes. Further randomized controlled studies with more participants are needed to evaluate the accurate effects of mAMH levels on preeclampsia and should increase the power of mAMH levels in predicting the preeclampsia.