Rama Vunnam

Background: Frequent PVCs have been associated with a reversible cardiomyopathy. Cutoffs of ≥ 10 000 PVCs/day and ≥ 15% PVCs have been suggested by the 2014 EHRA/HRS/APHRS and 2017 AHA/ACC/HRS Expert Consensus guidelines, respectively, for PVC suppression. Objective: To investigate the impact of PVC variability on meeting guideline‐suggested PVC thresholds. Methods: Six hundred and six patients with 14‐day ZIO monitor data sets with ≥ 10 000 PVCs on at least 1 day were identified (2014 guidelines cohort). Of these patients, 325 had at least 1 day of ≥ 15% PVCs (2017 guidelines cohort). Analysis was performed on these cohorts. Results: Within the 2014 guidelines cohort, mean daily PVC burden was 12 188 ± 8300 [range 0–64 188]. Intra‐patient daily PVCs were highly variable (median 3.6‐fold change between max and min PVC days (Q1/3: 2.22/10.15) with instances of > 10 000‐fold change observed. 54.3% and 19.5% of patients had days with < 5000 and < 1000 PVCs, respectively. Even patients with days of 0 PVCs (0.5%) were observed. Seventy‐two hours of monitoring detected 69% of patients with ≥ 10 000 PVCs/24 h with an additional 2%–4% of patients crossing the threshold each additional day. A bimodal distribution of the number of days meeting PVC thresholds/corresponding PVC counts was observed, suggesting a previously unidentified pattern of distinct populations—“low frequency/low PVC” (≤ 3/14 above‐threshold days/mean 12 342 PVCs those days) versus “high frequency/high PVC” (14/14 above‐threshold days/mean 24 580 PVCs those days). The 2017 guidelines cohort demonstrated similar findings. Conclusion: Daily PVC burdens vary greatly. More sensitive detection of guideline‐suggested cut‐offs requires prolonged monitoring. Novel potential PVC patterns may allow for better identification of candidates for PVC suppression.

Background Frequent PVCs have been associated with a reversible cardiomyopathy. Cutoffs of ≥10,000 PVCs/day and ≥15% PVCs have been suggested by the 2014 EHRA/HRS/APHRS and 2017 AHA/ACC/HRS Expert Consensus guidelines, respectively, for PVC suppression. Methods 606 patients with 14 day ZIO® monitor datasets with ≥10,000 PVCs on at least one day were identified (2014 Guidelines Cohort). Of these patients, 325 had at least one day of ≥15% PVCs (2017 Guidelines Cohort). Analysis was performed on these cohorts to investigate the impact of PVC variability on meeting guideline thresholds. Results Within the 2014 Guidelines Cohort, mean daily PVC burden was 12,188±8,300 [range 0-64,188]. Intra-patient daily PVCs were highly variable (median 3.6-fold change between max and min PVC days (Q1/3: 2.22/10.15) with instances of >10,000-fold change observed. 54.3% and 19.5% of patients had days with Conclusion Daily PVC burdens vary greatly. More sensitive detection of guideline-suggested cut-offs requires prolonged monitoring. Novel potential PVC patterns may allow for better identification of candidates for PVC suppression.

Purpose: We sought to study the predictive value of the metabolic heterogeneous zone (HZ) as determined by ¹⁸Fluorodeoxyglucose (¹⁸FDG) positron emission tomography (PET) viability studies in ventricular tachycardia (VT) patients.Methods: PET studies utilizing ⁸²Rubidium (⁸²Rb) tracer for perfusion and ¹⁸FDG tracer for viability were analyzed using PMOD (PMOD Technologies) and further analyzed using 684‐segment plots. ¹⁸FDG uptake was normalized to the area with maximal perfusion on the rest ⁸²Rb study. Metabolic scar, HZ, and healthy segments were defined with perfusion‐normalized ¹⁸FDG uptake between 0%–50%, 50%–70%, and >70%, respectively.Results: Thirty‐four VT patients (age, 63 ± 12 years) were evaluated with ¹⁸FDG‐PET viability study. Most (n = 31) patients underwent VT ablation. Patients were categorized to HZ < median versus HZ ≥ median based on a median HZ area size of 21.0 cm². HZ size was significantly larger in the deceased group than the alive group (35.2 cm² vs. 18.1 cm², p = .01). Deaths were significantly higher in HZ ≥ 21 cm² group than HZ < 21 cm² group (58.8% vs. 11.8%, p = .005). Survival analysis showed significantly higher mortality in the HZ ≥ 21 cm² group than the HZ < 21 cm² group (HR = 4.1, 95% CI: 1.3–12.6, p = .016). In a multivariable analysis, HZ was found to be an independent predictor for all‐cause mortality (HR = 1.07, 95% CI: 1.02–1.12, p = .01)Conclusions: Increased HZ size of myocardium was associated with increased mortality. Metabolic HZ quantification may be of value in risk stratification and management of ischemic and nonischemic patients with VT.

Background: Coronavirus disease 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus that was first discovered in December 2019 in Wuhan, China. With the growing numbers of community spread cases worldwide, the World Health Organization (WHO) declared the COVID-19 outbreak as a pandemic on March 11, 2020. Like influenza viruses, SARS-CoV-2 is thought to be mainly transmitted by droplets and direct contact, and COVID-19 has a similar disease presentation to influenza. Here we present a case of influenza A and COVID-19 co-infection in a 60-year-old man with end-stage renal disease (ESRD) on hemodialysis. Case presentation: A 60-year-old man with ESRD on hemodialysis presented for worsening cough, shortness of breath, and diarrhea. The patient first developed a mild fever (37.8 °C) during hemodialysis 3 days prior to presentation and has been experiencing worsening flu-like symptoms, including fever of up to 38.6 °C, non-productive cough, generalized abdominal pain, nausea, vomiting, and liquid green diarrhea. He lives alone at home with no known sick contacts and denies any recent travel or visits to healthcare facilities other than the local dialysis center. Rapid flu test was positive for influenza A. Procalcitonin was elevated at 5.21 ng/mL with a normal white blood cell (WBC) count. Computed tomography (CT) chest demonstrated multifocal areas of consolidation and extensive mediastinal and hilar adenopathy concerning for pneumonia. He was admitted to the biocontainment unit of Nebraska Medicine for concerns of possible COVID-19 and was started on oseltamivir for influenza and vancomycin/cefepime for the probable bacterial cause of his pneumonia and diarrhea. Gastrointestinal (GI) pathogen panel and Clostridioides difficile toxin assay were negative. On the second day of admission, initial nasopharyngeal swab came back positive for SARS-CoV-2 by real-time reverse-transcriptase polymerase chain reaction (RT-PCR). The patient received supportive care and resumed bedside hemodialysis in strict isolation, and eventually fully recovered from COVID-19. Conclusions: We presented a case of co-infection of influenza and SARS-CoV-2 in a hemodialysis patient. The possibility of SARS-CoV-2 co-infection should not be overlooked even when other viruses including influenza can explain the clinical symptoms, especially in high-risk patients.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent for the 2019 coronavirus disease (COVID-19) pandemic, has caused a public health emergency. The need for additional research in viral pathogenesis is essential as the number of cases and deaths rise. Understanding the virus and its ability to cause disease has been the main focus of current literature; however, there is much unknown. Studies have revealed new findings related to the full transmission potential of SARS-CoV-2 and its subsequent ability to cause infection by different means. The virus is hypothesized to be of increased virulence compared with previous coronavirus that caused epidemics, in part due to its overall structural integrity and resilience to inactivation. To date, many studies have discussed that the rationale behind its transmission potential is that viral RNA has unexpectedly been detected in multiple bodily fluids, with some samples having remained positive for extended periods of time. Additionally, the receptor by which the virus gains cellular entry, ACE2, has been found to be expressed in different human body systems, thereby potentiating its infection in those locations. In this evidence-based comprehensive review, we discuss various potential routes of transmission of SARS-CoV-2—respiratory/droplet, indirect, fecal-oral, vertical, sexual, and ocular. Understanding these different routes is important as they pertain to clinical practice, especially in taking preventative measures to mitigate the spread of SARS-CoV-2.

The severe acute respiratory syndrome virus (SARS-CoV-2), a novel coronavirus first discovered in Wuhan, China in December 2019 causes the Coronavirus Disease 19 (COVID-19), which presents with a wide range of clinical symptoms from mild or moderate to severe and critical illnesses. With the continuing transmission of the virus worldwide and the rapidly evolving situation globally, the World Health Organization (WHO) declared the COVID-19 outbreak a pandemic in March. Currently, there is no proven specific treatment for this potentially deadly disease beyond supportive care. However, a massive effort has been put globally into the investigation of medications and other interventional measures to fight COVID-19. Convalescent plasma therapy from recovered patients has recently drawn considerable interest. Several alternative medical treatments, although evidence of their efficacy still lacking, have also gained popularity, especially in countries with such traditions such as India and China. Rapid repurposing of drugs for COVID-19 has revealed a few promising candidate antiviral agents, but further research, especially high quality randomized controlled trials, will be needed to prove their efficacy and safety in the clinical use to treat COVID-19. Vaccine development has been the imperative task in the battle against SARS-CoV-2. While clinical trials have been launched for several candidate vaccines, research on COVID-19 vaccines is still at an early stage. So far, optimized supportive care remains the best practice against COVID-19.

Background: Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2, a novel coronavirus that was first discovered in Wuhan, China in December 2019. With the growing numbers of community spread cases worldwide, the World Health Organization (WHO) declared the COVID-19 outbreak as a pandemic on March 11. Like influenza viruses, SARS-CoV-2 is thought to be transmitted by contact, droplets, and fomites, and COVID-19 has a similar disease presentation to influenza. Here we present a case of influenza A and COVID-19 co-infection in a 60-year-old man with end-stage renal disease (ESRD) on hemodialysis.Case presentation: A 60-year-old man with ESRD on hemodialysis (HD) presented for worsening cough, shortness of breath, and diarrhea. The patient first developed a mild fever (100 °F) during hemodialysis three days prior to presentation and has been experiencing worsening flu-like symptoms, including fever of up to 101.6 °F, non-productive cough, generalized abdominal pain, nausea, vomiting, and liquid green diarrhea. He lives alone at home with no known sick contacts and denies any recent travel or visits to healthcare facilities other than the local dialysis center. Rapid flu test was positive for influenza A. Procalcitonin was elevated at 5.21 ng/mL with a normal white blood cell (WBC) count. Computed tomography (CT) chest demonstrated multifocal areas of consolidation and extensive mediastinal and hilar adenopathy concerning for pneumonia. He was admitted to the biocontainment unit of Nebraska Medicine for concerns of possible COVID-19 and was started on oseltamivir for influenza and vancomycin/cefepime for the probable bacterial cause of his pneumonia and diarrhea. GI pathogen panel and C. diff toxin assay were negative. On the second day of admission, initial nasopharyngeal swab came back positive for SARS-CoV-2 by RT-PCR. The patient received supportive care and resumed bedside hemodialysis in strict isolation, and eventually fully recovered from COVID-19.Conclusions: Our case demonstrated that co-infection of influenza and SARS-CoV-2 can occur in patients with no known direct exposure to COVID-19. The possibility of SARS-CoV-2 co-infection should not be overlooked even when other viruses including influenza can explain the clinical symptoms.

Background: Cardiac magnetic resonance (CMR) characteristics of ventricular radiofrequency ablation (RFA) lesions have only been incompletely defined.Aim: To determine the detectability and imaging characteristics of ventricular RFA lesions in an unselected patient cohort undergoing ventricular arrhythmia ablation.Methods and results: A retrospective chart review (n = 249) identified 36 patients with either pre‐/postablation CMR (n = 14) or only postablation CMR (n = 22). Ablation lesions could be identified in 50% (n = 18) of patients. Nonvisualized lesions had more preexisting transmural late gadolinium enhancement (LGE) >75% at the ablation sites (21% vs 0.0%, P = .042), more prevalent ICD artifact (50% vs 0%, P = .001), and lower ejection fraction (35.8 ± 14.2% vs 45.3 ± 13.4%, P = .048). Early CMR imaging demonstrated a central “black” signal void (microvascular obstruction [MVO], n = 12, 67%) up to 32 days post‐RFA, whereas late imaging showed a homogenously “white” gadolinium enhancement pattern (n = 6, 33%). MVO was only observed in nonfibrotic myocardium without preexisting LGE (n = 12) but was not observed in the scar with preexisting LGE (n = 3, P = .002) suggesting different wash‐in/wash‐out kinetics in scar/nonscar myocardium. Signal intensity (1909 vs 2534, P = .009) and contrast‐to‐noise ratio (−7.8 vs 16.3, P = .009) were significantly different between MVO and LGE lesions, respectively.Conclusion: Ventricular ablation lesions visualization is negatively affected by preexisting transmural scar, ICD artifact, and low ejection fraction. The transition of “black” MVO appearance to “white” LGE appearance on CMR occurs around 1 month following ablation, suggesting a change in histological characteristics of ablation lesions. This may affect the utility of CMR in the evaluation of the ventricular lesions, when undergoing real‐time or repeat VT ablations.

Introduction: Visualization of left atrial (LA) anatomy using image integration modules has been associated with decreased radiation exposure and improved procedural outcome when used for guidance of pulmonary vein isolation (PVI) in atrial fibrillation (AF) ablation. We evaluated the CARTOSEG™ CT Segmentation Module (Biosense Webster, Inc.) that offers a new CT‐specific semiautomatic reconstruction of the atrial endocardium.Methods: The CARTOSEG™ CT Segmentation Module software was assessed prospectively in 80 patients undergoing AF ablation. Using preprocedural contrast‐enhanced computed tomography (CE‐CT), cardiac chambers, coronary sinus (CS), and esophagus were semiautomatically segmented. Segmentation quality was assessed from 1 (poor) to 4 (excellent). The reconstructed structures were registered with the electroanatomic map (EAM). PVI was performed using the registered 3D images.Results: Semiautomatic reconstruction of the heart chambers was successfully performed in all 80 patients with AF. CE‐CT DICOM file import, semiautomatic segmentation of cardiac chambers, esophagus, and CS was performed in 185 ± 105, 18 ± 5, 119 ± 47, and 69 ± 19 seconds, respectively. Average segmentation quality was 3.9 ± 0.2, 3.8 ± 0.3, and 3.8 ± 0.2 for LA, esophagus, and CS, respectively.Registration accuracy between the EAM and CE‐CT‐derived segmentation was 4.2 ± 0.9 mm. Complications consisted of one perforation (1%) which required pericardiocentesis, one increased pericardial effusion treated conservatively (1%), and one early termination of ablation due to thrombus formation on the ablation sheath without TIA/stroke (1%). All targeted PVs (n = 309) were successfully isolated.Conclusions: The novel CT‐ CARTOSEG™ CT Segmentation Module enables a rapid and reliable semiautomatic 3D reconstruction of cardiac chambers and adjacent anatomy, which facilitates successful and safe PVI.