The cardiac intensive care unit and the cardiac intensivist during the COVID-19 surge in New York City.

Critical care cardiology has been impacted by the coronavirus disease-2019 (COVID-19) pandemic. COVID-19 causes severe acute respiratory distress syndrome, acute kidney injury, as well as several cardiovascular complications including myocarditis, venous thromboembolic disease, cardiogenic shock, and cardiac arrest. The cardiac intensive care unit is rapidly evolving as the need for critical care beds increases. Herein, we describe the changes to the cardiac intensive care unit and the evolving role of critical care cardiologists and other clinicians in the care of these complex patients affected by the COVID-19 pandemic. These include practical recommendations regarding structural and organizational changes to facilitate care of patients with COVID-19; staffing and personnel changes; and health and safety of personnel. We draw upon our own experiences at NewYork-Presbyterian Columbia University Irving Medical Center to offer insights into the unique challenges facing critical care clinicians and provide recommendations of how to address these challenges during this unprecedented time.

Cardiac Tumors: Clinical Presentation, Diagnosis, and Management.

OPINION STATEMENT: Cardiac masses and tumors are a heterogenous group of disorders and include primary tumors (both benign and malignant), metastatic disease, and numerous masquerades such as thrombus. Clinical presentation ranges from incidental discovery on imaging tests ordered for other reasons to life-threatening presentations such as cardiac tamponade, arrhythmia, obstruction, and systemic embolization. Of the available imaging modalities, cardiac MRI is generally the most useful for assessment and helps to delineate the relevant anatomy. Due to the technical difficulties and risk of biopsy of cardiac masses, a presumptive diagnosis is typically made using imaging techniques with surgery serving both a diagnostic and curative role. Because these conditions can vary widely in their management, we recommend early involvement of a multidisciplinary group which should include a cardiologist, cardiac surgeon, and oncologist.

Impact of the presence and extent of incomplete angiographic revascularization after percutaneous coronary intervention in acute coronary syndromes: the Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) trial.

BACKGROUND: The clinical significance of incomplete coronary revascularization (ICR) after percutaneous coronary intervention in patients with acute coronary syndromes is unknown. METHODS AND RESULTS: We performed quantitative angiography of the entire coronary tree in 2954 patients with acute coronary syndromes in the Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) trial. ICR was variably defined if any lesion with diameter stenosis (DS) cutoffs ranging from ≥30% to ≥70% with reference vessel diameter ≥2.0 mm remained after percutaneous coronary intervention. The primary outcome was 1-year composite rate of major adverse cardiac events (death, myocardial infarction, or ischemia-driven unplanned revascularization). With the use of DS cutoffs ≥30%, ≥40%, ≥50%, ≥60%, and ≥70%, the prevalence of ICR after percutaneous coronary intervention was 75%, 55%, 37%, 25%, and 17%, respectively. The 1-year major adverse cardiac event rate was increased among patients with ICR using all of the DS cutoffs. ICR (≥50% DS) was associated with higher 1-year rates of myocardial infarction (12.0% versus 8.2%; hazard ratio, 1.50; 95% confidence interval, 1.18-1.89; P=0.0007) and ischemia-driven unplanned revascularization (15.7% versus 10.2%; hazard ratio, 1.58; 95% confidence interval, 1.28-1.96; P<0.0001), with a trend toward increased mortality (3.1% versus 2.2%; hazard ratio, 1.43; 95% confidence interval, 0.90-2.27; P=0.13). By multivariable analysis, ICR (≥50% DS) was an independent predictor of 1-year major adverse cardiac events (hazard ratio, 1.36; 95% confidence interval, 1.12-1.64; P=0.002). The impact of ICR on major adverse cardiac events was similar regardless of chronic total occlusion presence, but it was more pronounced with a greater number of nonrevascularized lesions. CONCLUSIONS: Depending on the threshold of percent DS, ICR was present in 17% to 75% of patients with acute coronary syndromes after percutaneous coronary intervention. Regardless of the threshold, ICR was strongly associated with 1-year myocardial infarction, ischemia-driven unplanned revascularization, and major adverse cardiac events. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00093158.

Twelve hours of sustained ventricular fibrillation supported by a continuous-flow left ventricular assist device.

Left ventricular assist device (LVAD) therapy improves survival and quality of life by mechanically unloading the left ventricle and maintaining hemodynamics in patients with end-stage heart failure. LVADs can also be lifesaving by maintaining hemodynamics during ventricular arrhythmia. Continuous-flow LVADs have become the preferred LVAD technology. As presented here, a continuous-flow LVAD successfully provided hemodynamic support to a patient in sustained ventricular fibrillation for over 12 hours when the internal defibrillator was unable to terminate the arrhythmia. This case demonstrates that continuous-flow LVADs can be lifesaving in the setting of otherwise certain hemodynamic collapse from sustained ventricular fibrillation.

Intractable cardiac arrest due to lidocaine toxicity successfully resuscitated with lipid emulsion.

OBJECTIVE: Demonstrate a case report involving successful use of lipid emulsion therapy for intractable cardiac arrest due to lidocaine toxicity. DATA SOURCE: Lipid emulsion therapy has been shown to be effective in treating the cardiotoxic effects of such drugs as bupivacaine, verapamil, propranolol, and clomipramine as mentioned in a 2009 editorial in Critical Care Medicine by Jeffrey Bent. The mechanism of action of lipid emulsion therapy is not well defined and has been postulated to work by both a "lipid sink," decreasing circulating amounts of drugs to the periphery, or through a direct "energy source" to the myocardium. We present a case report of a patient successfully resuscitated with lipid emulsion therapy after prolonged and intractable lidocaine toxicity. Lidocaine is generally considered much less cardiotoxic than other local anesthetics and is used commonly as infusions for intractable ventricular arrhythmias. CONCLUSION: This case demonstrates the need to consider lipid emulsion therapy in the advanced cardiac life support algorithm for lidocaine toxicity as well as other lipid soluble drug intoxications.

Post-acute COVID-19 syndrome.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the pathogen responsible for the coronavirus disease 2019 (COVID-19) pandemic, which has resulted in global healthcare crises and strained health resources. As the population of patients recovering from COVID-19 grows, it is paramount to establish an understanding of the healthcare issues surrounding them. COVID-19 is now recognized as a multi-organ disease with a broad spectrum of manifestations. Similarly to post-acute viral syndromes described in survivors of other virulent coronavirus epidemics, there are increasing reports of persistent and prolonged effects after acute COVID-19. Patient advocacy groups, many members of which identify themselves as long haulers, have helped contribute to the recognition of post-acute COVID-19, a syndrome characterized by persistent symptoms and/or delayed or long-term complications beyond 4 weeks from the onset of symptoms. Here, we provide a comprehensive review of the current literature on post-acute COVID-19, its pathophysiology and its organ-specific sequelae. Finally, we discuss relevant considerations for the multidisciplinary care of COVID-19 survivors and propose a framework for the identification of those at high risk for post-acute COVID-19 and their coordinated management through dedicated COVID-19 clinics.

A Boulder in the Chest: Case of Massive Pulmonary Artery Sarcoma.

A 79-year-old woman presented with dyspnea and cough. Workup revealed a pulmonary artery mass. After undergoing surgery, she was treated with adjuvant immunotherapy for an undifferentiated pulmonary artery sarcoma. Fifteen months after surgery, there was no evidence of recurrence. The case is discussed, imaging presented, and the published reports reviewed. (Level of Difficulty: Intermediate.).

Electrical remodeling contributes to complex tachyarrhythmias in connexin43-deficient mouse hearts.

Loss of connexin43 (Cx43) gap junction channels in the heart results in a marked increase in the incidence of spontaneous and inducible polymorphic ventricular tachyarrhythmias (PVTs). The mechanisms resulting in this phenotype remain unclear. We hypothesized that uncoupling promotes regional ion channel remodeling, thereby increasing electrical heterogeneity and facilitating the development of PVT. In isolated-perfused control hearts, programmed electrical stimulation elicited infrequent monomorphic ventricular tachyarrhythmias (MVT), and dominant frequencies (DFs) during MVT were similar in the right ventricle (RV) and left ventricle (LV). Moreover, conduction properties, action potential durations (APDs), and repolarizing current densities were similar in RV and LV myocytes. In contrast, PVT was common in Cx43 conditional knockout (OCKO) hearts, and arrhythmias were characterized by significantly higher DFs in the RV compared to the LV. APDs in OCKO myocytes were significantly shorter than those from chamber-matched controls, with RV OCKO myocytes being most affected. APD shortening was associated with higher levels of sustained current in myocytes from both chambers as well as higher levels of the inward rectifier current only in RV myocytes. Thus, alterations in cell-cell coupling lead to regional changes in potassium current expression, which in this case facilitates the development of reentrant arrhythmias. We propose a new mechanistic link between electrical uncoupling and ion channel remodeling. These findings may be relevant not only in cardiac tissue but also to other organ systems where gap junction remodeling is known to occur.

Incidence, predictors, and impact of neurological events in non-ST-segment elevation acute coronary syndromes: the ACUITY trial.

AIMS: We sought to describe the incidence, predictors, and impact of adverse neurological events (NE) in a non-ST-segment elevation acute coronary syndromes (NSTEACS) population undergoing percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG), or medical therapy (MT). METHODS AND RESULTS: 13,819 patients with moderate and high-risk NSTEACS were enrolled in the prospective ACUITY trial. Angiography was performed within 72 hours of presentation, after which 7,789 patients (56.4%) underwent PCI, 1,539 (11.1%) underwent CABG, and 4,491 (32.5%) received MT. The rate of NE (stroke or transient ischaemic attack) at 30 days and one year and its relationship to adverse ischaemic events, including death, were assessed. Thirty-day rates of NE were 1.1% with CABG, 0.3% with PCI, and 0.5% with MT (p<0.001). One-year rates of NE were 1.1% with CABG, 0.3% with PCI, and 0.6% with MT (p<0.001). Independent predictors of NE at 30 days and one year included age, renal insufficiency, baseline troponin elevation, and initial treatment with CABG. The occurrence of NE was a strong independent predictor of death at 30 days and one year (HR 4.07, 95% CI [1.49, 11.11], p=0.006, and HR 4.25, 95% CI [2.37, 7.62], p<0.001, respectively). CONCLUSIONS: In the large-scale ACUITY trial, CABG was associated with a higher risk of NE at 30 days and one year compared to PCI and MT. The occurrence of NE in patients with NSTEACS was strongly associated with increased early and late mortality. Clinical Trials.gov Identifier NCT00093158.

Combat hypoxia: the importance of airway management & oxygenation of the traumatic brain injury patient.

Brain injury, specifically TBI, is a common occurrence in our society, with devastating physical, emotional, social and economic costs. Injury not only occurs on initial impact, but also develops slowly over ensuing hours or days. TBI poses unique challenges and requires special care, especially with airway management and ventilatory treatment. Serial assessment, particularly of the GCS and pupillary changes, is vital in continuing to monitor patient status. All treatment associated with the TBI patient is aimed at restoring CPP and allowing oxygenated blood to reach injured brain tissues.

The Concept of "Burden" in Atrial Fibrillation.

Over the last decade or so the term "burden" has become frequently encountered in manuscripts discussing atrial fibrillation (AF). AF "burden" is perhaps most commonly encountered in the electrophysiological context - the amount of time the patient is in AF out of the total monitored time (i.e., the percent of time one is in AF). However, "burden" in AF may also be used in other contexts, which we characterize below as "disease burden", "clinical burden," "economic burden." Over the course of the disease progression and its therapy, such "burdens" may change, and may do so in parallel with each other or in opposite directions. This manuscript explores these various concepts of AF "burden" so as to emphasize to authors and readers that when using the term, its meaning must be made clear.

Updating an institutional chest pain algorithm: incorporating new evidence on emerging pharmacotherapy.

Clinical treatment pathways are useful to ensure that evidence-based medicine is consistently applied in hospital systems and have been shown to improve patient outcomes. Such pathways need to be regularly updated and revised by incorporating new evidence from clinical trials to ensure optimal clinical care. In 2011, we published the Columbia University Medical Center/New York Presbyterian Hospital - Clinical Pathways for Acute Coronary Syndromes and Chest Pain. This algorithm includes primary percutaneous coronary intervention for all patients with ST-segment elevation myocardial infarction and an early invasive approach for patients with non-ST-segment elevation myocardial infarction. Since our last chest pain algorithm update, the novel antiplatelet agent ticagrelor has been introduced in the United States, resulting in an important revision of our acute coronary syndrome clinical pathways. Herein, we present our updated chest pain algorithm and provide rationale for the changes that we have made to our protocol.

Quantification and impact of untreated coronary artery disease after percutaneous coronary intervention: the residual SYNTAX (Synergy Between PCI with Taxus and Cardiac Surgery) score.

OBJECTIVES: The purpose of this study was to quantify the extent and complexity of residual coronary stenoses following percutaneous coronary intervention (PCI) and to evaluate its impact on adverse ischemic outcomes. BACKGROUND: Incomplete revascularization (IR) after PCI is common, and most studies have suggested that IR is associated with a worse prognosis compared with complete revascularization (CR). However, formal quantification of the extent and complexity of residual atherosclerosis after PCI has not been performed. METHODS: The baseline Synergy Between PCI With Taxus and Cardiac Surgery (SYNTAX) score (bSS) from 2,686 angiograms from patients with moderate- and high-risk acute coronary syndrome (ACS) undergoing PCI enrolled in the prospective ACUITY (Acute Catheterization and Urgent Intervention Triage Strategy) trial was determined. The SS after PCI was also assessed, generating the "residual" SS (rSS). Patients with rSS >0 were defined as having IR and were stratified by rSS tertiles, and their outcomes were compared to the CR group. RESULTS: The bSS was 12.8 ± 6.7, and after PCI the rSS was 5.6 ± 2.2. Following PCI, 1,084 patients (40.4%) had rSS = 0 (CR), 523 (19.5%) had rSS >0 but ≤2, 578 (21.5%) had rSS >2 but ≤8, and 501 patients (18.7%) had rSS >8. Age, insulin-treated diabetes, hypertension, smoking, elevated biomarkers or ST-segment deviation, and lower ejection fraction were more frequent in patients with IR compared with CR. The 30-day and 1-year rates of ischemic events were significantly higher in the IR group compared with the CR group, especially those with high rSS. By multivariable analysis, rSS was a strong independent predictor of all ischemic outcomes at 1 year, including all-cause mortality (hazard ratio: 1.05, 95% confidence interval: 1.02 to 1.09, p = 0.006). CONCLUSIONS: The rSS is useful to quantify and risk-stratify the degree and complexity of residual stenosis after PCI. Specifically, rSS >8.0 after PCI in patients with moderate- and high-risk ACS is associated with a poor 30-day and 1-year prognosis. (Comparison of Angiomax Versus Heparin in Acute Coronary Syndromes; NCT00093158).

Myocardial parvovirus B19 persistence: lack of association with clinicopathologic phenotype in adults with heart failure.

BACKGROUND: Multiple viruses have been isolated from the heart, but their significance remains controversial. We sought to determine the prevalence of cardiotropic viruses in endomyocardial biopsy (EMB) samples from adult patients with heart failure (HF) and to define the clinicopathologic profile of patients exhibiting viral positivity. METHODS AND RESULTS: EMB from 100 patients (median ejection fraction, 30%; interquartile range [IQR], 20% to 45%) presenting for cardiomyopathy evaluation (median symptom duration, 5 months; IQR, 1 to 13 months) were analyzed by polymerase chain reaction for adenovirus, cytomegalovirus, enteroviruses, Epstein-Barr virus, and parvovirus B19. Each isolate was sequenced, and viral load was determined. Parvovirus B19 was the only virus detected in EMB samples (12% of subjects). No patient had antiparvovirus IgM antibodies, but all had IgG antibodies, suggesting viral persistence. The clinical presentation of parvovirus-positive patients was markedly heterogeneous with both acute and chronic HF, variable ventricular function, and ischemic cardiomyopathy. No patient met Dallas histopathologic criteria for active or borderline myocarditis. Two patients with a positive cardiac MRI and presumed "parvomyocarditis" had similar viral loads to autopsy controls without heart disease. The oldest parvovirus-positive patients were positive for genotype 2, suggesting lifelong persistence in the myocardium. CONCLUSIONS: Parvovirus B19 was the only virus isolated from EMB samples in this series of adult patients with HF from the United States. Positivity was associated with a wide array of clinical presentations and HF phenotypes. Our studies do not support a causative role for parvovirus B19 persistence in HF and, therefore, advocate against the use of antiviral therapy for these patients.

Reduced intercellular coupling leads to paradoxical propagation across the Purkinje-ventricular junction and aberrant myocardial activation.

Ventricular tachycardia is a common heart rhythm disorder and a frequent cause of sudden cardiac death. Aberrant cell-cell coupling through gap junction channels, a process termed gap junction remodeling, is observed in many of the major forms of human heart disease and is associated with increased arrhythmic risk in both humans and in animal models. Genetically engineered mice with cardiac-restricted knockout of Connexin43, the major cardiac gap junctional protein, uniformly develop sudden cardiac death, although a detailed electrophysiological understanding of their profound arrhythmic propensity is unclear. Using voltage-sensitive dyes and high resolution optical mapping techniques, we found that uncoupling of the ventricular myocardium results in ectopic sites of ventricular activation. Our data indicate that this behavior reflects alterations in source-sink relationships and paradoxical conduction across normally quiescent Purkinje-ventricular muscle junctions. The aberrant activation profiles are associated with wavefront collisions, which in the setting of slow conduction may account for the highly arrhythmogenic behavior of Connexin43-deficient hearts. Thus, the extent of gap junction remodeling in diseased myocardium is a critical determinant of cardiac excitation patterns and arrhythmia susceptibility.