Faculty Bibliography

BACKGROUND:Videoscopic left cardiac sympathetic denervation (LCSD) is an adjunct therapy for reduction of arrhythmia-induced events in patients with long-QT syndrome (LQTS). LCSD reduces LQTS-triggered breakthrough cardiac events. The temporal effects of QTc changes post-LCSD have not been studied. METHODS:We utilized continuous QTc monitoring on 72 patients with LQTS. We evaluated acute and long-term QTc changes in comparison to 12-lead ECG-derived QTc values prior to surgery, 24 hours postsurgery, and at follow up ≥3 months. RESULTS:Seventy-two patients underwent LCSD at our institution (46% male, mean age at LCSD was 14 ± 10 years). The mean baseline, pre-LCSD QTc was 505 ± 56 ms, which had decreased significantly at ≥3 months post-LCSD to 491 ± 40 ms (P = 0.001). QTc monitoring revealed that the majority of the cohort (53/72; 74%) had a transient increase >30 ms in QTc from baseline, with an average maximum increase of 72 ± 30 ms. Resolution within 10 ms of baseline or less occurred in 57% (30/53) at 24 hours post-LCSD. CONCLUSIONS:Although LQTS patients may have a paradoxically increased QTc post-LCSD, the effects are transient in most patients. Importantly, no patients experienced any arrhythmias in the postoperative setting related to this transient rise in QTc.

Although rotational parameters by speckle tracking echocardiography (STE) have been previously compared to sonomicrometry and cardiac magnetic resonance imaging, few have examined the relationship between left ventricular (LV) rotational mechanics and intraventricular measures of load-independent contractility, LV stiffness, or ventriculoarterial coupling. The aim of this study was to compare the changes in LV rotational indices to intraventricular pressure-volume (PV) relationships under a range of inotropic states induced by pharmacological interventions, acute ischemia, and changes in preload. In nine pigs, simultaneous echocardiographic imaging and LVPV measurements were performed during pharmacologically induced high or low inotropy and during acute ischemia by ligation of the left anterior descending coronary artery (LAD). Maximal ventricular elastance (Emax), arterial elastance (Ea), ventricular-arterial coupling (Emax/Ea), dP/dt, tau, and other hemodynamic parameters were determined. Dobutamine and esmolol infusions led to inversely correlated changes in hemodynamic measurements of LV function. Apical but not basal rotation and diastolic rotation rate were decreased by esmolol and increased by dobutamine. The LV twist correlates well with Emax (r = 0.83) and Emax/Ea (r = 0.80). Apical diastolic rotation rate also correlates with dP/dtmin (r = -0.63), Ï„ (r = -0.81), and LV stiffness (r = -0.52). LAD ligation decreased systolic and diastolic LV rotation in apical (P < 0.05), but not basal myocardium. Occlusion of the inferior vena cava, to reduce preload, increased apical rotation in systole and diastole. LV rotational parameters measured by STE provide quantitative and reproducible indices of global LV systolic and diastolic function during acute changes in hemodynamics.

BACKGROUND:A patent foramen ovale (PFO) may permit arterial embolization of thrombi that accumulate on the leads of cardiac implantable electronic devices in the right-sided cardiac chambers. We sought to determine whether a PFO increases the risk of stroke/transient ischemic attack (TIA) in patients with endocardial leads. METHODS AND RESULTS/RESULTS:We retrospectively evaluated all patients who had endocardial leads implanted between January 1, 2000, and October 25, 2010, at Mayo Clinic Rochester. Echocardiography was used to establish definite PFO and non-PFO cohorts. The primary end point of stroke/TIA consistent with a cardioembolic etiology and the secondary end point of mortality during postimplantation follow-up were compared in PFO versus non-PFO patients with the use of Cox proportional hazards models. We analyzed 6075 patients (364 with PFO) followed for a mean 4.7 ± 3.1 years. The primary end point of stroke/TIA was met in 30/364 (8.2%) PFO versus 117/5711 (2.0%) non-PFO patients (hazard ratio, 3.49; 95% confidence interval, 2.33-5.25; P<0.0001). The association of PFO with stroke/TIA remained significant after multivariable adjustment for age, sex, history of stroke/TIA, atrial fibrillation, and baseline aspirin/warfarin use (hazard ratio, 3.30; 95% confidence interval, 2.19-4.96; P<0.0001). There was no significant difference in all-cause mortality between PFO and non-PFO patients (hazard ratio, 0.91; 95% confidence interval, 0.77-1.07; P=0.25). CONCLUSIONS:In patients with endocardial leads, the presence of a PFO on routine echocardiography is associated with a substantially increased risk of embolic stroke/TIA. This finding suggests a role of screening for PFOs in patients who require cardiac implantable electronic devices; if a PFO is detected, PFO closure, anticoagulation, or nonvascular lead placement may be considered.

While right ventricular (RV) dysfunction has long been known to affect the performance of left ventricle (LV), the mechanisms remain poorly defined. Recently, speckle-tracking echocardiography has demonstrated that preservation of strain and rotational dynamics is crucial to both LV systolic and diastolic function. We hypothesized that alteration in septal strain and rotational dynamics of the LV occurs during acute RV pressure overload (RVPO) and leads to decreased cardiac performance. Seven anesthetized pigs underwent median sternotomy and placement of intraventricular pressure-volume conductance catheters. Two-dimensional echocardiographic images and LV pressure-volume loops were acquired for offline analysis at baseline and after banding of the pulmonary artery to achieve RVPO (>50 mmHg) induced RV dysfunction. RVPO resulted in a significant decrease (P < 0.05) in LV end-systolic elastance (50%), systolic change in pressure over change in time (19%), end-diastolic volume (22%), and cardiac output (37%) that correlated with decrease in LV global circumferential strain (58%), LV apical rotation (28%), peak untwisting (reverse rotation) rate (27%), and prolonged time to peak rotation (17%), while basal rotation was not significantly altered. RVPO reduced septal radial and circumferential strain, while no other segment of the LV midpapillary wall was affected. RVPO decreased septal radial strain on LV side by 27% and induced a negative radial strain from 28 ± 5 to -16 ± 2% on the RV side of the septum. The septal circumferential strain on both LV and RV side decreased by 46 and 50%, respectively, following RVPO (P < 0.05). Our results suggest that acute RVPO impairs LV performance by primarily altering septal strain and apical rotation.

A quarter of patients with implanted cardiac devices have a patent foramen ovale (PFO). Thrombus is frequently noted on intravascular leads that in the presence of a PFO could result in cerebral vascular embolic events. However, whether this mechanism of stroke occurs is not clearly known. We report three patients with PFO, implanted leads with thrombus, and stroke, including a patient where thrombus partially attached to the lead was seen traversing the PFO.

Augmentation of cardiac sympathetic tone during myocardial ischemia has been shown to increase myocardial O(2) demand and infarct size as well as induce arrhythmias. We have previously demonstrated that electroacupuncture (EA) inhibits the visceral sympathoexcitatory cardiovascular reflex. The purpose of this study was to determine the effects of EA on left ventricular (LV) function, O(2) demand, infarct size, arrhythmogenesis, and in vivo cardiac norepinephrine (NE) release in a myocardial ischemia-reperfusion model. Anesthetized rabbits (n = 36) underwent 30 min of left anterior descending coronary artery occlusion followed by 90 min of reperfusion. We evaluated myocardial O(2) demand, infarct size, ventricular arrhythmias, and myocardial NE release using microdialysis under the following experimental conditions: 1) untreated, 2) EA at P5-6 acupoints, 3) sham acupuncture, 4) EA with pretreatment with naloxone (a nonselective opioid receptor antagonist), 5) EA with pretreatment with chelerythrine (a nonselective PKC inhibitor), and 6) EA with pretreatment with both naloxone and chelerythrine. Compared with the untreated and sham acupuncture groups, EA resulted in decreased O(2) demand, myocardial NE concentration, and infarct size. Furthermore, the degree of ST segment elevation and severity of LV dysfunction and ventricular arrhythmias were all significantly decreased (P < 0.05). The cardioprotective effects of EA were partially blocked by pretreatment with naloxone or chelerythrine alone and completely blocked by pretreatment with both naloxone and chelerythrine. These results suggest that the cardioprotective effects of EA against myocardial ischemia-reperfusion are mediated through inhibition of the cardiac sympathetic nervous system as well as opioid and PKC-dependent pathways.