The inflammatory response triggered by sepsis can frequently cause reversible myocardial depression termed sepsis-induced cardiomyopathy. The resulting pathologic changes are often self-limiting and cardiac function returns to baseline following resolution of the underlying exacerbating factors. The following case examines a patient with septic shock and sepsis-induced cardiomyopathy that, despite maximal medical therapy, required mechanical support with an Impella assist device for seven days. To the best of our knowledge and research, this represents the longest documented use of an Impella heart pump in septic shock and associated sepsis-induced cardiomyopathy. Utilization of mechanical support in the setting of septic shock has seen growing interest in recent years, but more structured studies need to be conducted for better understanding of their overall effect on morbidity and mortality.
Introduction: Obstructive sleep apnea (OSA) effects up to 30% of men and 15% of women in North America. Untreated, OSA is associated with the development of hypertension, heart failure, coronary artery disease, cardiac arrhythmia, and stroke. Treatment reduces these risks. The American Academy of Sleep Medicine outlines the first line treatment of OSA as continuous positive airway pressure (CPAP). However, many patients are unable to tolerate CPAP. One of the newest therapies approved in 2014 is implantation of a hypoglossal nerve stimulator (HNS) which functions by stimulating the tongue protrudor muscles to reduce upper airway obstruction. However, there is minimal research investigating HNS's effects on comorbidities. Currently there are two published studies showing improved blood pressure control and heart rate variability, but each study only included 46 patients. Several factors warrant a comparison including the lack of data, procedural risks, and procedural cost; especially, when considering the proven efficacy and low cost of CPAP. We present a retrospective analysis of blood pressure after HNS implantation. Hypothesis: We hypothesize that HNS implantation will improve blood pressure control. Methods: All cases of HNS implantation at MercyOne North Iowa Mason City, Iowa were retrospectively reviewed. Each case was manually reviewed for pre- and post-surgery blood pressure, heart failure exacerbations, arrhythmia, hemoglobin A1c, stroke, and acute coronary syndrome. Results: Fifty-nine patients had a mean change in blood pressure of +1.76 systolic and +0.76 diastolic with a standard error of 2.10 and 1.29 respectively. The mean follow-up time was 5.7 months after the fine-tuning sleep titration study. Five patients needed one less blood pressure medication and 6 patients needed one more. Preliminary regression analysis does not support gender, age, apnea-hypopnea index, or body mass index being predictive of change in blood pressure with HNS implantation. There was no statistically significant effect on other comorbidities. Conclusion: This study showed no clinically significant change in blood pressure after HNS implantation. Limitations include the small sample size and only one follow-up blood pressure.
Left ventricular(LV) thrombus results from Virchow's triad with factors such as reduced wall motion, reduced ejection fraction, and myocardial injury contributing to clot formation. While the prevalence is relatively low in the general population with an incidence of 7/10,000 patients, it can complicate up to 39% of anterior MIs. Serious adverse complications can result from LV thrombus including systemic thromboembolism and stroke. To reduce this risk, anticoagulation is the mainstay of treatment. Historically, LV thrombus was treated with vitamin K antagonists. The American and European guidelines recommend oral anticoagulant therapy with warfarin with varying durations from 3-6 months. However, there are no prospective trials comparing warfarin and direct oral anticoagulants(DOACs) as anticoagulation in the treatment of LV thrombus. Current research includes one meta-analysis of only 8 retrospective studies demonstrating non-inferiority of DOACs compared to warfarin. We present further evidence to suggest the noninferiority of DOACs vs warfarin in the treatment of LV thrombus. METHODS:We reviewed all cases of LV thrombus at two facilities in Iowa, United States. Echocardiogram reports were electronically searched for the inclusion terms "ventricular thrombus," "LV thrombus," and "apical thrombus." Each report was then individually reviewed for accuracy and ejection fraction. Individual patient charts were reviewed for selected anticoagulation at the time of diagnosis, for follow-up echocardiograms, and for adverse events including thromboembolism, gastrointestinal bleed, and death. As this was a retrospective nonrandomized chart analysis, the decision to prescribe VKA vs DOAC was largely based on physician preference. Follow-up echocardiogram reports were reviewed for resolution and ejection fraction. Resolution was defined as complete absence of LV thrombus by the next echocardiogram as interpreted by the echocardiographer.RESULTS: Seventy-six patients were included in the study. Fifty-six received warfarin and twenty-three received a DOAC. Resolution was seen in 68% of patients treated with warfarin and in 65% of patients treated with a DOAC. The average ejection fraction at the time of diagnosis and at the time of resolution are listed respectively: warfarin resolved 38% and 40%, warfarin unresolved 29% and 34%, DOAC resolved 35% and 36%, DOAC unresolved 36% and 38%. The average time to follow-up was 147 days (range 9 -681). Complications of gastrointestinal bleed and stroke did not reach statistical significance.CONCLUSIONS: This retrospective study again suggests DOACs are non-inferior compared to warfarin in the treatment of left ventricular thrombus in our population in Iowa, United States.CLINICAL IMPLICATIONS: This data emphasizes the need for a prospective randomized clinical trial to determine the most effective and safe treatment strategy for LV thrombus.
We present a case report of a patient presenting with subarachnoid hemorrhage whose electrocardiogram (ECG) mimicked non-ST-elevation myocardial infarction. A 36-year-old male with a past medical history of resistant hypertension, previous severe acute respiratory syndrome coronavirus 2 infection, and alcohol abuse presented to the hospital after cardiac arrest. He was taken to the catheterization lab upon arrival and was found to have an unremarkable coronary angiogram. After angiography, computerized tomography (CT) head was performed revealing an acute, large-volume, subarachnoid hemorrhage. Subsequent CT angiogram of the head confirmed this with source noted to be a ruptured aneurysm of the anterior communicating artery. ST depression on ECG has been reported in patients who have suffered a subarachnoid hemorrhage. Although the most common etiology of cardiac arrest is an acute coronary syndrome, other etiologies based on a patient's past medical history need to remain in the differential. Recognition of ECG changes may lead to earlier diagnosis and decreased mortality in subarachnoid patients.
Background and SignificanceRecent evidence suggests aberrant carotid body chemoreceptor (CBC) function contributes to tonic elevation of renal nerve activity and reductions in renal blood flow in chronic heart failure (CHF). These changes combined with anemia and capillary rarefaction likely contribute to tissue hypoxia, and may drive renal fibrosis and attendant dysfunction. Previous work indicates that stable expression of hypoxia‐inducible factor 1‐α (HIF1α) and down regulation of MiR‐155 drive gene programs that mediate epithelial‐mesenchymal transition (EMT) in renal tubular epithelial cells, including increases in Krüppel‐like factor 4 (KLF4) and matrix metalloproteinase 9 (MMP9). To date, no studies have examined this signaling pathway in CHF, thus our objective was to determine the influence of CBC on renal cortical expression of HIF1α, KLF4, MiR‐155, MMP9, and α‐smooth muscle actin (SMA) in CHF.HypothesisWe hypothesize that CBC‐mediated reductions in renal blood flow activate EMT pathways in CHF by exacerbating tissue hypoxia, leading to sustained accumulation of HIF1α, downregulation of MiR‐155, and KLF4/MMP9/SMA induction.MethodsTo address this hypothesis, we measured expression of HIF1α, MiR‐155, KLF4, MMP9, and SMA in renal cortical tissue from sham, and CHF animals (n=4–8 per group) with and without ablation of the CBC (CBA). CHF was induced in rats by coronary artery ligation (CAL) and CBA was performed (4 weeks post‐CAL) by cryogenic ablation. CHF was confirmed via echocardiography under isoflurane anesthesia (1–1.5%). At 8‐weeks post‐CAL, rats were humanely euthanized and renal cortical tissue was collected and analyzed for HIF1α, KLF4, MMP9, and SMA expression via western blot and MiR‐155 expression by RT‐qPCR.ResultsEjection fraction was 72±2% in sham animals, 34±2% in CHF animals, and 32±2% in CHF‐CBA animals (p<0.05 sham vs. CHF and CHF‐CBA). Expression of HIF1α was 1.37±0.33 in CHF rats relative to sham, and 1.25±0.15 in CHF‐CBA relative to sham. KLF4 was 1.64±0.25 in CHF rats relative to sham, and this effect was attenuated in CHF‐CBA (1.06±0.16 relative to sham, p<0.05 vs. CHF). MMP9 expression in CHF rats was 1.79±0.43 relative to sham and 1.092±0.23 in CHF‐CBA relative to sham. SMA expression in CHF rats was 0.58±0.17 relative to sham and 0.83±0.15 relative to sham in CHF‐CBA. MiR‐155 expression in CHF rats was 0.48±0.11 relative to sham, and this effect was attenuated by CBA (0.73±0.12 relative to sham, p<0.05 vs. CHF).ConclusionThese results suggest a novel relationship between CBC function and expression of renal cortical MiR‐155 and KLF4 in CHF, and that CBA has the potential to influence EMT pathways in the kidney in this pathophysiological setting.Support or Funding InformationThis work was supported by a grant from NHLBI (1 R15 HL138600‐01)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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