Leukemic Infiltration of Myocardium Presenting as Cardiac Arrest.
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ABSTRACT:
SUBMITTER: Torosyan N
PROVIDER: S-EPMC8311278 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Acute coronary syndromes (ACS) usually occur in patients with multiple cardiac risk factors. In young adults, drug use and hypercoagulable states are common causes for ACS presentations. We report a case of a man in his early 30s who was diagnosed with polycythemia vera (PV) and had a cardiac arrest due to an anterolateral ST elevation myocardial infarction. We discuss his unique management and review the evidence on the management of arterial thromboembolism in PV patients.
| S-EPMC6362489 | biostudies-literature
Project description:BackgroundSudden cardiac arrest (SCA) is a major contributor to mortality, but data are limited among nonwhites. Identification of differences in clinical profile based on race may provide opportunities for improved SCA prevention.Methods and resultsIn the ongoing Oregon Sudden Unexpected Death Study (SUDS), individuals experiencing SCA in the Portland, OR, metropolitan area were identified prospectively. Patient demographics, arrest circumstances, and pre-SCA clinical profile were compared by race among cases from 2002 to 2012 (for clinical history, n=126 blacks, n=1262 whites). Incidence rates were calculated for cases from the burden assessment phase (2002-2005; n=1077). Age-adjusted rates were 2-fold higher among black men and women (175 and 90 per 100 000, respectively) compared with white men and women (84 and 40 per 100 000, respectively). Compared with whites, blacks were >6 years younger at the time of SCA and had a higher prearrest prevalence of diabetes mellitus (52% versus 33%; P<0.0001), hypertension (77% versus 65%; P=0.006), and chronic renal insufficiency (34% versus 19%; P<0.0001). There were no racial differences in previously documented coronary artery disease or left ventricular dysfunction, but blacks had more prevalent congestive heart failure (43% versus 34%; P=0.04) and left ventricular hypertrophy (77% versus 58%; P=0.02) and a longer QTc interval (466±36 versus 453±41 milliseconds; P=0.03).ConclusionsIn this US community, the burden of SCA was significantly higher in blacks compared with whites. Blacks with SCA had a higher prearrest prevalence of risk factors beyond established coronary artery disease, providing potential targets for race-specific prevention.
| S-EPMC4526124 | biostudies-literature
Project description:Post-cardiac arrest myocardial dysfunction is a common phenomenon after return of spontaneous circulation (ROSC) and contributes to hemodynamic instability and low survival rates after cardiac arrest. Mild hypothermia for 24 h after ROSC has been shown to significantly improve neurologic recovery and survival rates. In the present study we investigate the influence of therapeutic hypothermia on hemodynamic parameters in resuscitated patients and on contractility in failing human myocardium. We analyzed hemodynamic data from 200 cardiac arrest survivors during the hypothermia period. The initial LVEF was 32.6 +/- 1.2% indicating a significantly impaired LV function. During hypothermia induction, the infusion rate of epinephrine could be significantly reduced from 9.1 +/- 1.3 microg/min [arrival intensive care unit (ICU) 35.4 degrees C] to 4.6 +/- 1.0 microg/min (34 degrees C) and 2.8 +/- 0.5 microg/min (33 degrees C). The dobutamine and norepinephrine application rates were not changed significantly. The mean arterial blood pressure remained stable. The mean heart rate significantly decreased from 91.8 +/- 1.7 bpm (arrival ICU) to 77.3 +/- 1.5 bpm (34 degrees C) and 70.3 +/- 1.4 bpm (33 degrees C). In vitro we investigated the effect of hypothermia on isolated ventricular muscle strips from explanted failing human hearts. With decreasing temperature, the contractility increased to a maximum of 168 +/- 23% at 27 degrees C (n = 16, P < 0.05). Positive inotropic response to hypothermia was accompanied by moderately increased rapid cooling contractures as a measure of sarcoplasmic reticulum (SR) Ca(2+) content, but can be elicited even when the SR Ca(2+) release is blocked in the presence of ryanodine. Contraction and relaxation kinetics are prolonged with hypothermia, indicating increased Ca(2+) sensitivity as the main mechanism responsible for inotropy. In conclusion, mild hypothermia stabilizes hemodynamics in cardiac arrest survivors which might contribute to improved survival rates in these patients. Mechanistically, we demonstrate that hypothermia improves contractility in failing human myocardium most likely by increasing Ca(2+)-sensitivity.
| S-EPMC2858797 | biostudies-literature
Project description:BackgroundThere is limited data regarding long-term survival in patients who present with STEMI and out of hospital cardiac arrest (OHCA).MethodsWe prospectively analysed outcomes in 3521 consecutive patients who were diagnosed with STEMI and underwent primary percutaneous coronary intervention (PPCI) or coronary artery bypass surgery from 2004 to 2017. They were divided into two groups according to the presence of cardiac arrest (group I, patients with cardiac arrest; n = 156 group II, patients without cardiac arrest; n = 3365).ResultsPatients with OHCA had higher in hospital mortality (27.7% vs 2.9%, p < 0.01), sustained VT or VF (44.6% vs 4.3%, p < 0.01) and cardiogenic shock (22.9% vs 6.8%, p < 0.01). 30-day mortality (excluding death within first 24 h) was also higher in the OHCA group (24.6% vs 3.3%, p < 0.01). There was no significant difference in recurrent AMI, TVR, stroke, major bleeds or new onset heart failure. After a mean follow-up of 18.6 months, mortality was higher in patients with OHCA (7.9% vs 3.8%, p 0.04). This was driven mainly by an increase in cardiac mortality (5% vs 1.1%, p < 0.01). OHCA was a significant predictor of mortality beyond 30 days (HR - 2.5, 95% CI 0.99-6.3). Kaplan-Meier curves and the log-rank test revealed that patients with OHCA had significantly lower survival (p < 0.01).ConclusionsPatients with STEMI complicated by OHCA remain a high-risk group associated with high in hospital mortality. Beyond 30 days the occurrence of cardiac arrest was a significant predictor of all-cause and cardiac mortality.
| S-EPMC6305836 | biostudies-literature
Project description:Limited data regarding the prognostic impact of ventricular tachyarrhythmias related to out-of-hospital (OHCA) compared to in-hospital cardiac arrest (IHCA) is available. A large retrospective single-center observational registry with all patients admitted due to ventricular tachyarrhythmias was used including all consecutive patients with ventricular tachycardia (VT) and fibrillation (VF) on admission from 2002 to 2016. Survivors discharged after OHCA were compared to those after IHCA using multivariable Cox regression models and propensity-score matching for evaluation of the primary endpoint of long-term all-cause mortality at 2.5 years. Secondary endpoints were all-cause mortality at 6 months and cardiac rehospitalization at 2.5 years. From 2.422 consecutive patients with ventricular tachyarrhythmias, a total of 524 patients survived cardiac arrest and were discharged from hospital (OHCA 62%; IHCA 38%). In about 50% of all cases, acute myocardial infarction was the underlying disease leading to ventricular tachyarrhythmias with consecutive aborted cardiac arrest. Survivors of IHCA were associated with increased long-term all-cause mortality compared to OHCA even after multivariable adjustment (28% vs. 16%; log rank p = 0.001; HR 1.623; 95% CI 1.002-2.629; p = 0.049) and after propensity-score matching (28% vs. 19%; log rank p = 0.045). Rates of cardiac rehospitalization rates at 2.5 years were equally distributed between OHCA and IHCA survivors. In patients presenting with ventricular tachyarrhythmias, survivors of IHCA were associated with increased risk for all-cause mortality at 2.5 years compared to OHCA survivors.
| S-EPMC8986738 | biostudies-literature
Project description:Background The study sought to assess the prognostic impact of acute myocardial infarction ( AMI ) with and without ST -segment-elevation myocardial infarction ( STEMI and NSTEMI ) in patients with ventricular tachyarrhythmias and sudden cardiac arrest ( SCA ) on admission. Methods and Results A large retrospective registry was used including all consecutive patients presenting with ventricular tachycardia ( VT ), fibrillation ( VF ), and sudden cardiac arrest ( SCA ) on admission from 2002 to 2016. AMI versus non- AMI and STEMI versus NSTEMI were compared applying multivariable Cox regression models and propensity-score matching for evaluation of the primary prognostic end point defined as long-term all-cause mortality at 2.5 years. Secondary end points were 30 days all-cause mortality, cardiac death at 24 hours, in hospital death, and recurrent percutaneous coronary intervention (re- PCI ) at 2.5 years. In 2813 unmatched high-risk patients with ventricular tachyarrhythmias and SCA , AMI was present in 29% (10% STEMI , 19% NSTEMI ) with higher rates of VF (54% versus 31%) and SCA (35% versus 26%), whereas VT rates were higher in non- AMI (56% versus 30%) ( P < 0.05). AMI -related VT ≥48 hours was associated with higher mortality (log rank P = 0.001). Multivariable Cox regression models revealed non- AMI (hazard ratio = 1.458; P = 0.001) and NSTEMI (hazard ratio = 1.460; P = 0.036) associated with increasing long-term all-cause mortality at 2.5 years, which was also proven after propensity-score matching (non- AMI versus AMI : 55% versus 43%, log rank P = 0.001, hazard ratio = 1.349; NSTEMI versus STEMI : 45% versus 34%, log rank P = 0.047, hazard ratio = 1.372). Secondary end points including 30 days and in-hospital mortality, as well as re- PCI were higher in non- AMI patients. Conclusions In high-risk patients presenting with ventricular tachyarrhythmias and SCA , non- AMI revealed higher mortality than AMI , respectively NSTEMI than STEMI , alongside AMI -related VT ≥48 hours.
| S-EPMC6404887 | biostudies-literature
Project description: Not available
| S-EPMC9314221 | biostudies-literature
Project description:Background High-mobility group box 1 (HMGB1) is a major promotor of ischemic injuries and aseptic inflammatory responses. We tested its inhibition on neurological outcome and systemic immune response after cardiac arrest (CA) in rabbits. Methods and Results After 10 minutes of ventricular fibrillation, rabbits were resuscitated and received saline (control) or the HMGB1 inhibitor glycyrrhizin. A sham group underwent a similar procedure without CA. After resuscitation, glycyrrhizin blunted the successive rises in HMGB1, interleukin-6, and interleukin-10 blood levels as compared with control. Blood counts of the different immune cell populations were not different in glycyrrhizin versus control. After animal awakening, neurological outcome was improved by glycyrrhizin versus control, regarding both clinical recovery and histopathological damages. This was associated with reduced cerebral CD4+ and CD8+ T-cell infiltration beginning 2 hours after CA. Conversely, granulocytes' attraction or loss of microglial cells or cerebral monocytes were not modified by glycyrrhizin after CA. These modifications were not related to the blood-brain barrier preservation with glycyrrhizin versus control. Interestingly, the specific blockade of the HMGB1 receptor for advanced glycation end products by FPS-ZM1 recapitulated the neuroprotective effects of glycyrrhizin. Conclusions Our findings support that the early inhibition of HMGB1-signaling pathway prevents cerebral chemoattraction of T cells and neurological sequelae after CA. Glycyrrhizin could become a clinically relevant therapeutic target in this situation.
| S-EPMC9973651 | biostudies-literature
Project description:Previous studies have identified multiple risk factors that are associated with total cardiac mortality. Nevertheless, identifying specific factors that distinguish patients at risk of arrhythmic death versus heart failure could better target patients likely to benefit from implantable cardiac defibrillators, which have no impact on nonsudden cardiac death.We performed a pilot competing risks analysis of the National Institutes of Health-sponsored PAREPET trial (Prediction of Arrhythmic Events with Positron Emission Tomography). Death from cardiac causes was ascertained in subjects with ischemic cardiomyopathy (n=204) eligible for an implantable cardiac defibrillator for the primary prevention of sudden cardiac arrest after baseline clinical evaluation and imaging at enrollment (positron emission tomography and 2-dimensional echo). Mean age was 67±11 years with an ejection fraction of 27±9%, and 90% were men. During 4.1 years of follow-up, there were 33 sudden cardiac arrests (arrhythmic death or implantable cardiac defibrillator discharge for ventricular fibrillation or ventricular tachycardia >240 bpm) and 36 nonsudden cardiac deaths. Sudden cardiac arrest was correlated with a greater volume of denervated myocardium (defect of the positron emission tomography norepinephrine analog 11C-hydroxyephedrine), lack of angiotensin inhibition therapy, elevated B-type natriuretic peptide, and larger left ventricular end-diastolic volume index. In contrast, nonsudden cardiac death was associated with a higher resting heart rate, older age, elevated creatinine, larger left atrial volume index, and larger left ventricular end-diastolic volume index.Distinct clinical, laboratory, and imaging variables are associated with cause-specific cardiac mortality in primary-prevention candidates with ischemic cardiomyopathy. If prospectively validated, these multivariable associations may help target specific therapies to those at the greatest risk of sudden and nonsudden cardiac death.URL: https://clinicaltrials.gov. Unique identifier: NCT01400334.
| S-EPMC5555076 | biostudies-literature
Project description:Ischemic heart disease (IHD) and dilated cardiomyopathy (DCM) are the two most common etiologies of heart failure (HF). Both forms share common characteristics including ventricle dilation in the final stage. Immune mechanisms in HF are increasingly highlighted and have been implicated in the pathogeneses of IHD and DCM. A better understanding of adhesion molecule expression and correlated immune cell infiltration could enhance disease detection and improve therapeutic targets. This study was performed to explore the common mechanisms underlying IHD and DCM. After searching the Gene Expression Omnibus database, we selected the GSE42955, GSE76701, GSE5406, GSE133054 and GSE57338 datasets for different expressed gene (DEGs) selection and new cohort establishment. We use xcell to calculate immune infiltration degree, ssGSEA and GSEA to calculate the pathway and biological enrichment score, consensus cluster to identify the m6A modification pattern, and LASSO regression to make risk predicting model and use new combined cohort to validate the results. The screening stage revealed that vascular cell adhesion molecule 1 (VCAM1) play pivotal roles in regulating DEGs. Subsequent analyses revealed that VCAM1 was differentially expressed in the myocardium and involved in regulating immune cell infiltration. We also found that dysregulated VCAM1 expression was associated with a higher risk of HF by constructing a clinical risk-predicting model. Besides, we also find a connection among the m6A RNA modification ,expression of VCAM1 and immune regulation. Those connection can be linked by the Wnt pathway enrichment alternation. Collectively, our results suggest that VCAM-1 have the potential to be used as a biomarker or therapy target for HF and the m6A modification pattern is associated with the VCAM1 expression and immune regulation.
| S-EPMC8484263 | biostudies-literature