Electrical storm after left ventricular assist device (LVAD) implantation.

INTRODUCTION: Ventricular tachycardia storm or electrical storm (ES) is a common complication following left ventricular assist device (LVAD) implantation. The factors contributing to ES and outcomes are less studied. The study aimed to determine the factors associated with ES and the probability of survival in patients undergoing LVAD in three tertiary centers over a span of 15 years. METHODS: We performed a retrospective cohort study on all patients who underwent LVAD implantation at the Mayo Clinic (Rochester, Phoenix, and Jacksonville) from January 1, 2006 to December 31, 2020. ES was defined as ≥3 episodes of sustained ventricular tachycardia over a period of 24 h with no identifiable reversible cause. Detailed chart reviews of the electronic health records within the Mayo Clinic and outside medical records were performed. RESULTS: A total of 883 patients who underwent LVAD implantation were included in our study. ES occurred in 7% (n = 61) of patients with a median of 13 days (interquartile range [IQR]: 5-297 days) following surgery. We found 57% of patients (n = 35) developed ES within 30 days, while 43% (n = 26) patients developed ES at a median of 545  (IQR 152-1032) days after surgery. Following ES, 26% of patients died within 1 year. Patients with ES had a significant association with a history of ventricular arrhythmias and implantable cardioverter defibrillator (ICD) shocks before the procedure. ES was significantly associated with reduced survival compared to patients without ES (hazards ratio [HR]: 1.92, 95% CI: 1.39-2.64, p < .001). CONCLUSION: Following LVAD implantation, the rate of ES was 7% with majority of ES occurring within 30 days of LVAD. Risk factors for ES included pre-implant history of ventricular arrhythmias and ICD shock. ES was significantly associated with reduced survival compared to patients without ES.

The electrocardiographic manifestations of pectus excavatum before and after surgical correction.

BACKGROUND: Pectus excavatum (PEx) can cause cardiopulmonary limitations due to cardiac compression and displacement. There is limited data on electrocardiogram (ECG) alterations before and after PEx surgical repair, and ECG findings suggesting cardiopulmonary limitations have not been reported. The aim of this study is to explore ECG manifestations of PEx before and after surgery including associations with exercise capacity. METHODS: A retrospective review of PEx patients who underwent primary repair was performed. ECGs before and after surgical correction were evaluated and the associations between preoperative ECG abnormalities and cardiopulmonary function were investigated. RESULTS: In total, 310 patients were included (mean age 35.1 ± 11.6 years). Preoperative ECG findings included a predominant negative P wave morphology in V1, and this abnormal pattern significantly decreased from 86.9% to 57.4% (p < 0.001) postoperatively. The presence of abnormal P wave amplitude in lead II (>2.5 mm) significantly decreased from 7.1% to 1.6% postoperatively (p < 0.001). Right bundle branch block (RBBB) (9.4% versus 3.9%, p < 0.001), rsr' patterns (40.6% versus 12.9%, p < 0.001), and T wave inversion in leads V1-V3 (62.3% vs 37.7%, p < 0.001) were observed less frequently after surgery. Preoperative presence of RBBB (OR = 4.8; 95%CI 1.1-21.6) and T wave inversion in leads V1-3 (OR = 2.3; 95%CI 1.3-4.2) were associated with abnormal results in cardiopulmonary exercise testings. CONCLUSION: Electrocardiographic abnormalities in PEx are frequent and can revert to normal following surgery. Preoperative RBBB and T wave inversion in leads V1-3 suggested a reduction in exercise capacity, serving as a marker for the need for further cardiovascular evaluation of these patients.

Decitabine Induced Delayed Cardiomyopathy in Hematologic Malignancy.

Decitabine is a pyrimidine analogue of nucleoside cytidine, used for the treatment of myelodysplastic syndromes, chronic myelogenous leukemia, and acute myelogenous leukemia. We present a case of cardiomyopathy associated with decitabine used for secondary acute myelogenous leukemia. The patient presented with new heart failure symptoms and an ejection fraction decline.

Left atrial appendage exclusion during mitral valve surgery and stroke in atrial fibrillation.

PURPOSE: The purpose of this study was to determine whether surgical left atrial appendage (LAA) exclusion performed during mitral valve surgery is associated with a reduction in cerebrovascular events in patients with atrial fibrillation. METHODS: We retrospectively studied patients with atrial fibrillation who underwent mitral valve surgery from 1/1/2001 through 12/31/2014. We screened 1352 patients using ICD-9 codes and included 281 patients in the study. The primary end point was a composite of strokes and transient ischemic attacks occurring within 5 years after surgery. Secondary end points were stroke, transient ischemic attack, and all-cause mortality. RESULTS: The LAA exclusion group (n = 188) had a lower prevalence of female gender, hypertension, and diabetes mellitus compared with the non-LAA exclusion group (n = 93). The CHA2DS2VASc scores were comparable between groups (2.6 vs 2.9, P = .11), as was anticoagulant use (82.4% vs 85.0%, P = .60). Concomitant surgical ablation was performed in 73.9% of patients who underwent LAA exclusion. Nine cerebrovascular events occurred in the LAA exclusion group and 13 in the non-LAA exclusion group (HR 0.30 [0.12-0.75], P = .01). There was no difference in all-cause mortality between groups. On multivariate analysis of the primary end point of strokes or transient ischemic attacks, significant variables were LAA exclusion (HR 0.31 [0.12-0.76], P = .01) and CHA2DS2VASc score (HR 1.44 [1.11-1.87], P = .006). The benefit of LAA exclusion was detected only when performed together with surgical ablation (HR 0.27 [0.09-0.72], P = .01). CONCLUSIONS: LAA exclusion was associated with fewer cerebrovascular events. However, this benefit was seen only with concomitant surgical ablation.

Brugada syndrome and its relevance in the perioperative period.

Brugada syndrome is an autosomal dominant genetic disorder associated with an increased risk of sudden cardiac death, as well as ventricular tachyarrhythmias.The defective cardiac sodium channels result in usual electrocardiographic findings of a coved-type ST elevation in precordial leads V1 to V3. The majority of patients have uncomplicated courses with anesthesia, surgery, and invasive procedures. However there is risk of worsening ST elevation and ventricular arrhythmias due to perioperative medications, surgical insult, electrolyte abnormalities, fever, autonomic nervous system tone, as well as other perturbations. Given the increasing numbers of patients with inherited conduction disorders presenting for non-cardiac surgery that are at risk of sudden cardiac death, safe anesthetic management depends upon a detailed knowledge of these conditions.

Erdheim-Chester disease: The role of video-assisted thoracoscopic surgery in diagnosing and treating cardiac involvement.

INTRODUCTION: Erdheim-Chester disease is a rare, non-Langerhans histiocytosis in which pericardial involvement is diagnosed with increasing frequency and is associated with high mortality rates. PRESENTATION OF CASE: A 53-year-old woman presented with progressive exertional dyspnea and pericardial effusion was discovered. Further investigations revealed the presence of a diffuse, infiltrating process and a diagnosis of Erdheim-Chester disease was made. An emergent pericardiocentesis by subxiphoid approach was completed but recurrent drainage obviated removal of the pigtail catheter. A pleuro-pericardial window was placed using video-assisted thoracoscopic surgery (VATS) and analysis of the resected specimen confirmed pericardial involvement. DISCUSSION: In this case, high pericardial fluid output demanded definitive treatment of the pericardial effusion. Traditionally this would be completed via thoracotomy. VATS is a minimally invasive alternative which permits exploration of the thoracic cavity and the creation of a pleuropericardial window. CONCLUSION: We describe, for the first time, the successful use of VATS for both diagnostic confirmation and therapeutic relief of recurrent pericardial fluid drainage due to pericardial involvement by Erdheim-Chester disease.

Syncope while driving: clinical characteristics, causes, and prognosis.

BACKGROUND: The risk of syncope occurring while driving has obvious implications for personal and public safety. We aimed to define the clinical characteristics, causes, and prognosis of syncope while driving. METHODS AND RESULTS: In this case-control study of consecutive patients evaluated for syncope from 1996 through 1998 at an academic medical center, we documented causes, clinical characteristics, and recurrence of syncope while driving. Of 3877 patients identified, 381 (9.8%) had syncope while driving (driving group). Compared with the 3496 patients (90.2%) who did not have syncope while driving, the driving group was younger (P=0.01) and had higher percentages of male patients (P<0.001) and patients with a history of any cardiovascular disease (P=0.01) and stroke (P=0.02). Syncope while driving was commonly caused by neurally mediated syncope (37.3%) and cardiac arrhythmias (11.8%). Long-term survival in the driving group was comparable to that of an age- and sex-matched cohort from the Minnesota population (P=0.15). Among the driving group, syncope recurred in 72 patients, 35 of whom (48.6%) had recurrence >6 months after the initial evaluation. Recurrences during driving happened in 10 patients in the driving group, 7 of which (70%) were >12 months after the initial evaluation. CONCLUSIONS: In our study, neurally mediated syncope was the most common type of syncope while driving. The causes of syncope, the late recurrences of syncope (during > or =6 months of follow-up), and the overall low incidence of recurrent syncope while driving provide useful information to supplement current recommendations on driving for these patients.

Independent association between obstructive sleep apnea and subclinical coronary artery disease.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with coronary risk factors, but it is unknown if OSA is associated with development of coronary disease. We evaluated the association between OSA and the presence of subclinical coronary disease assessed by coronary artery calcification (CAC). METHODS: Consecutive patients with no history of coronary disease who underwent electron-beam CT within 3 years of polysomnography between March 1991 and December 2003 were included. OSA was defined by an apnea-hypopnea index (AHI) > or = 5 events per hour, and patients were grouped by quartiles of AHI severity. Logistic regression modeled the association between OSA severity and presence of CAC. RESULTS: There were 202 patients (70% male; median age, 50 years; mean body mass index, 32 kg/m(2); 8% diabetic; 9% current smokers; 60% hypercholesterolemic; and 47% hypertensive). OSA was present in 76%. CAC was present in 67% of OSA patients and 31% of non-OSA patients (p < 0.001). Median CAC scores (Agatston units) were 9 in OSA patients and 0 in non-OSA patients (p < 0.001). Median CAC score was higher as OSA severity increased (p for trend by AHI quartile < 0.001). With multivariate adjustment, the odds ratio for CAC increased with OSA severity. Using the first AHI quartile as reference, the adjusted odds ratios for the second, third, and fourth quartiles were 2.1 (p = 0.12), 2.4 (p = 0.06), and 3.3 (p = 0.03), respectively. CONCLUSIONS: In patients without clinical coronary disease, the presence and severity of OSA is independently associated with the presence and extent of CAC. OSA identifies patients at risk for coronary disease and may represent a highly prevalent modifiable risk factor.