Incidence Of Myocardial Damage Research Articles

A Multicentric Observational Study to Determine Myocardial Injury in Severe Community-Acquired Pneumonia (sCAP).

Background: Severe community-acquired pneumonia (sCAP) is the most frequent admission for acute respiratory failure in intensive care medicine. Observational studies have found a correlation between patients who were admitted with CAP and the development of cardiovascular events. The risk of acute myocardial damage in patients with CAP is particularly high within the first 30 days of hospitalization. Research design and methods: Multicenter prospective cohort analysis conducted in consecutive patients admitted to an ICU with microbiologically confirmed diagnoses of sCAP. The aim was to determine any structural cardiac damage detected by advanced imagining techniques (cardiac MRI) and cardiac biomarkers in patients with sCAP. The patients were stratified, according to their etiology, into pneumococcal or not-pneumococcal sCAP. The primary outcome was cardiac damage at day 5 and 7 of clinical presentation. Results: A total of 23 patients were consecutively and prospectively enrolled for two winter periods. No significant differences were observed between the median troponin when comparing the pneumococcal vs. non-pneumococcal. The incidence of myocardial damage was numerically higher in the pneumococcal subgroup (70% vs. 50%, p = 0.61) on day 5 and on day 7 (53% vs. 40%, p = 0.81) but did not achieve significance. Confirming a correlation between the biomarkers of cell damage and the biomarkers of myocardial damage, only a positive and significant correlation was observed between h-FABP and DNA on day 1 (r = 0.74; p < 0.01) and day 3 (r = 0.83; p < 0.010). Twenty cardiac MRIs were performed on the 23 patients (87%). No presence of fibrosis was observed in any of the studies carried out within the first 15 days of admission. Conclusions: No significant myocardial damage was found in patients with sCAP independent of the bacterial etiology in accordance with biomarker alterations (Troponin and/or h-FABP) or cardiac MRI. Using cardiac MRI, we could not find any presence of myocardial fibrosis within the first 15 days of admission.

Clinical characteristics of community-acquired pneumonia in children caused by mycoplasma pneumoniae with or without myocardial damage: A single-center retrospective study.

Mycoplasma pneumoniae (MP) is a prevalent pathogen that causes respiratory infections in children and adolescents. To assess the differences in the clinical features of MP-associated community-acquired pneumonia (CAP) in children who presented with mild or severe mycoplasma pneumoniae pneumonia (MPP); to identify the incidence of myocardial damage between the two groups. This work is a retrospective study. We identified children between 2 mo and 16 years of age with clinical and radiological findings consistent with CAP. We admitted patients to the inpatient department of the Second Hospital of Jilin University, Changchun, China, from January 2019 to December 2019. A total of 409 hospitalized patients were diagnosed with MPP. Among them were 214 (52.3%) males and 195 (47.7%) females. The duration of fever and cough was the longest in severe MPP cases. Similarly, plasma levels of highly sensitive C-reactive protein (t = -2.834, P < 0.05), alanine transaminase (t = -2.511, P < 0.05), aspartate aminotransferase (t = -2.939, P < 0.05), and lactate dehydrogenase (LDH) (t = -2.939, P < 0.05) were all elevated in severe MPP cases compared with mild MPP cases, and these elevations were statistically significant (P < 0.05). Conversely, the neutrophil percentage was significantly lower in severe MPP cases than in mild MPP cases. The incidence of myocardial damage was significantly higher in severe MPP cases than in mild MPP cases (χ2 = 157.078, P < 0.05). Mycoplasma pneumoniae is the main cause of CAP. The incidence of myocardial damage was higher and statistically significant in severe MPP cases than in mild MPP cases.

CARDIOVASCULAR INVOLVEMENT AND MORTALITY WITH NEW COVID-19 VARIANTS

Objectives: The presence of cardiac involvement is accepted as an indicator of morbidity and mortality in Coronavirus disease 2019 (COVID-19) patients. Therefore, this study investigates data on cardiovascular involvement and clinical outcomes between the first wave with wild virus and mutation-dominant second wave of the COVID-19 outbreak. Methodology: This was a single centre, retrospective study using and the data was collected from confirmed COVID-19 patients. Patients’ demographic and clinical characteristics, cardiovascular involvement, and the factors associated with mortality were analysed. All these data were compared between first (wild virus) and second-wave (mutant viruses) patients. Results: The study included 476 positive inpatients confirmed by a real-time polymerase chain reaction. Although the length of hospital stay was similar, the duration of intensive care units (ICUs) was longer in the second wave (6.3 ± 3.2 vs. 7.5 ± 3.5; p=0.020). The rate of severe illness (12.9 vs. 20.3%; p=0.037) and critical illness referral to ICUs (4.3 vs. 9.7%; p=0.031) was higher in the second wave than in the first. In addition, the incidence of myocardial damage was significantly higher in the second wave (4.3 vs. 10.7%; p=0.046). Conclusion: In the present study, myocardial injury, development of critical illness, and referral to the ICUs increased in correlation with the disease severity in the second wave compared to the first. Variant viruses and possibly the burden of the crowd on healthcare contribute to this situation. Therefore, epidemiological data are required to guide situational awareness as long as the pandemic remains.

Explore of Hyperbaric Oxygen Therapy on the Patients with Acute Encephalopathy Scondery Myocardial Damage Following Carbon Monoxide Poising

Objective: To investigate the myocardial damage and hyperbaric oxygen treatment of acute encephalopathy in CO poisoning. Methods: Since March 2015 - March 2020 admitted to 125 patients with acute CO poisoning encephalopathy, emergency admission GCS score 7-8 points or less, and the intracranial pressure, myocardial damage markers enzymes (CK - MB, CK, LDH, MYO, BNP) and troponin (cTnl), arterial COHb quantitative and electrocardiogram (EKG) dynamic inspection, row CT, MRI examination can at the same time, using air pressure cabin HBO treatment, Each patient choose 2.5-3 period of treatment (Every10 times is a course of treatment), 99.5-100% oxygen purity (liquid oxygen gasification), oxygen supply time 60 minutes or 80 minutes, interlude 10 minutes. Results: The higher the COHb, the deeper the coma, the increased intracranial pressure, the intracranial hypertension, and the morphological changes such as diffuse cerebral edema and symmetrical globulin necrosis were observed in 125 patients. However, the myocardial damaging enzymes and troponin markers were significantly increased and the EKG abnormalities were basically consistent. HBO treatment achieved remarkable curative effect, the incidence of delayed encephalopathy was significantly reduced, and no death occurred. Conclusion: Increased intracranial pressure induced by acute encephalopathy induced by CO poisoning can significantly increase the incidence of myocardial damage, subendocardial myocardial infarction, left heart failure and various arrhythmias. HBO is a treatment for etiology and should be preferred.

Complicated AMI in a COVID-19 Patient; Chordal Rupture and Flail of Mitral Valve

: The incidence of myocardial damage in patients infected with coronavirus, as demonstrated by high levels of cardiac enzymes, electrocardiography (ECG) and trans-thoracic echocardiographic (TTE) problems is not clear. However it is associated with a more severe type of disease. Also, unlike most myocardial injuries seen in routine patients, it is not always due to thrombotic events. Hence, the reason for the injury has been hypothesized to be due to various factors including plaque rupture, viral cytokine storm, hypoxic injury, coronary spasms, micro-thrombi, or direct endothelial injury induced by the virus. Here we report a case of acute myocardial infarction in the setting of COVID-19, complicated with flail of the posterior mitral valve leaflet.

Abstract WP131: Correlation of Cardiac Derangement in Patients with Right-Sided Ischemic Stroke and the Severity of Insular Damage

Objective: Although it is known that neurogenic cardiac damage can occur after an ischemic stroke, the mapping of the neuroanatomic correlation of ischemic stroke-related myocardial injury remains to be defined. Our previous animal study found a higher incidence of myocardial damage from left-sided insular infarction comparing to the right side. However, the results from various clinical studies have been inconclusive. This clinical study aims to identify a quantitative correlation between adverse cardiac outcomes and insular infarction, left-sided versus right-sided, as well as potential prognostic factors that may be used to aid in assessing patient outcomes and making treatment decisions. Methods and Results: A serial measurements of cardiac troponin T (cTnT) and creatine phosphokinase-MB (CK-MB), 12-lead EKG, and two- dimensional echocardiography were performed in 42 patients with MRI-confirmed ischemic stroke involving the insular cortex. The severity of insular damage was measured with diffusion-weighted imaging studies (DWI). Patients with renal failure, recent cardiac ischemic events, or congestive heart failure were excluded. Twenty-two patients (52.4%) had left-sided middle cerebral artery (MCA) infarcts with insular involvement, whereas 20 (47.6%) had a right-sided MCA infarcts involving the insular cortex. When compared to patients with left MCA infarcts involving the insular cortex, patients with right MCA infarcts with insular involvement had significantly higher levels of cTnT elevation. By using the linear regression analysis we also identified a statistically significant correlation between cTnT elevation and severity of right insular damage, instead of the NIH stroke score (NIHSS) as commonly assumed. Moreover, two patients were found to have transient left ventricular wall hypokinesis which mimics Takotsubo cardiomyopathy. Conclusions: This study showed that patients with right MCA ischemic stroke involving the insular cortex, comparing to those with left-sided insular stroke, tend to have more severe cardiac insult leading to higher levels of cTnT. The study also identified severity of insular damage as a potential prognostic factor in assessing cardiac derangement as a complication of insular infarction.

Safety of fluvastatin in patients undergoing high-risk non-cardiac surgery

Importance of the field: In patients undergoing vascular surgery there is a high incidence of adverse cardiac events, due to sudden coronary plaque rupture. The non-lipid lowering or pleiotropic effects of statins can help reduce adverse cardiovascular events associated with vascular surgery.Areas covered in this review: The evidence for perioperative use of fluvastatin, as well as other statins, in high-risk surgery patients is summarized in this review. Data on pharmacokinetics and metabolism is presented, together with considerations on possible drug interactions in the perioperative period.What the reader will gain: The reader will gain a comprehensive understanding of the existing safety and efficacy data for fluvastatin and other statins in the perioperative period. The practical considerations of perioperative fluvastatin therapy will be presented, including potential side-effects and management of the early non-oral phase immediately post surgery. Finally, advice on when to initiate therapy and safety recommendations are offered.Take home message: In patients scheduled for high-risk vascular surgery, fluvastatin improves postoperative outcome, reducing the incidence of myocardial damage by ∼ 50% in the first 30 days following vascular surgery. In comparison with placebo, fluvastatin was not associated with a rise in liver enzymes or creatine kinase levels. To bridge the non-oral phase, an extended-release formula is recommended.

Influence of platelet reactivity and response to clopidogrel on myocardial damage following percutaneous coronary intervention in patients with non-st-segment elevation acute coronary syndrome

Introduction A wide variability in the response to clopidogrel and magnitude of post-treatment platelet reactivity has been described. However, this has been demonstrated by light transmittance aggregometry, a method too laborious for daily practice. Point-of-care devices may overcome this limitation, but little is known on the predictive value of such measurements. Our objective was to determine the relationship between platelet reactivity and the incidence of myocardial damage following percutaneous coronary intervention (PCI) in patients with Non-ST-segment Elevation Acute Coronary Syndrome (NSTEACS). Materials and Methods This prospective study included 93 patients with NSTEACS and PCI. All patients received a loading dose of 300 mg of clopidogrel and 250 mg of aspirin. Myocardial damage was defined as any elevation above upper limit of normal or previous levels of troponin T, assessed every 6 h for at least 24 h following PCI. Platelet reactivity not related to clopidogrel (BASE reactivity), related to P2Y12 inhibition (P2Y12 reactivity) and inhibition of platelet aggregation (IPA) were assessed immediately pre-PCI with the VerifyNow® device. Results Myocardial damage was detected in 60 patients (64.5%). Higher BASE reactivity was associated with myocardial damage (287.8 ± 62.6 vs. 260 ± 55.9 units, p = 0.043) while a trend was found for P2Y12 reactivity (173.4 ± 70.3 vs. 149.2 ± 58.4 units, p = 0.109). No relationship was detected for IPA. Multivariate logistic regression analysis confirmed that BASE reactivity (p = 0.04) and P2Y12 reactivity (p = 0.03) were independent predictors of myocardial damage. Conclusions Platelet reactivity before PCI appears to be better predictor of myocardial damage than does response to clopidogrel.

Regarding “A prospective study of subclinical myocardial damage in endovascular versus open repair of infrarenal abdominal aortic aneurysms”

Background Endovascular repair of abdominal aortic aneurysms (AAAs) is considered to be less invasive and better tolerated by the cardiovascular system than open repair. Our aim was to assess the true incidence of perioperative myocardial damage associated with endovascular vs open infrarenal AAA repair. Methods Between July 1999 and June 2001, preoperative and postoperative serum troponin T (TnT) levels were measured in all patients presenting for elective AAA repair at Royal Prince Alfred Hospital. The incidence of myocardial damage was recorded on the basis of standard clinical, biochemical, and electrocardiographic changes or a subclinical increase of 50% or more in serum TnT. Patients were excluded if the TnT increase was associated with a significant increase of serum creatinine (≥50%) with no other evidence of myocardial ischemia. The differences between the two groups were analyzed with the χ 2 test and odds ratios. Results A total of 35 open and 112 endovascular AAA repairs were included in the study. There was no significant difference in age, sex, preoperative serum creatinine, or preoperative serum TnT between the two treatment groups. Seventeen patients had biochemical evidence of myocardial damage, which was clinically obvious in only one patient. Even though the incidence of previous myocardial infarction was significantly higher in patients undergoing endovascular repair (41%) than open repair (22%; P P Conclusions There is a previously underestimated incidence of subclinical myocardial damage associated with surgery for infrarenal AAA which is lower after endovascular than open repair.

A prospective study of subclinical myocardial damage in endovascular versus open repair of infrarenal abdominal aortic aneurysms

Endovascular repair of abdominal aortic aneurysms (AAAs) is considered to be less invasive and better tolerated by the cardiovascular system than open repair. Our aim was to assess the true incidence of perioperative myocardial damage associated with endovascular vs open infrarenal AAA repair. Between July 1999 and June 2001, preoperative and postoperative serum troponin T (TnT) levels were measured in all patients presenting for elective AAA repair at Royal Prince Alfred Hospital. The incidence of myocardial damage was recorded on the basis of standard clinical, biochemical, and electrocardiographic changes or a subclinical increase of 50% or more in serum TnT. Patients were excluded if the TnT increase was associated with a significant increase of serum creatinine (> or =50%) with no other evidence of myocardial ischemia. The differences between the two groups were analyzed with the chi 2 test and odds ratios. A total of 35 open and 112 endovascular AAA repairs were included in the study. There was no significant difference in age, sex, preoperative serum creatinine, or preoperative serum TnT between the two treatment groups. Seventeen patients had biochemical evidence of myocardial damage, which was clinically obvious in only one patient. Even though the incidence of previous myocardial infarction was significantly higher in patients undergoing endovascular repair (41%) than open repair (22%; P < .05), the overall incidence of myocardial damage (clinical or subclinical) was significantly higher in the open group compared with the endovascular group (8 [25%] of 32 vs 9 [8%] of 109, respectively; odds ratio, 3.7; 95% confidence interval, 1.28-10.49; P < .02). There is a previously underestimated incidence of subclinical myocardial damage associated with surgery for infrarenal AAA which is lower after endovascular than open repair.

Estimation of myocardial damage in Kawasaki disease using antimyosin antibody.

In a retrospective study, 121 children with Kawasaki disease (KD) were investigated to determine (i) the incidence of myocardial damage using the antimyosin antibody (AMA) titer; (ii) the differences in the electrocardiograms between the AMA-positive and -negative patients; and (iii) the effect of treatment with intravenous gamma globulin (IVGG) on the AMA. Comparisons were made with 117 normal children (controls). Patients with KD showed a significantly higher mean AMA titer and more patients were positive for AMA than the controls. The AMA titer in the KD group was not related to the presence of coronary artery lesions. Electrocardiograms obtained during the acute and the convalescent stage of KD revealed that patients positive for AMA had a significantly lower voltage of T wave in lead V6 at week four than at week two of illness, whereas patients negative for AMA showed no T wave change after week two. The group treated with IVGG showed a significantly lower AMA titer than that not given IVGG. These observations suggest that myocardial damage occurs in some patients with KD which is unrelated to the presence of coronary artery lesions and that the treatment with IVGG reduces the AMA titer in patients with KD.

Frequency of myocardial indium-111 antimyosin uptake after uncomplicated coronary artery bypass grafting

The reported incidence of myocardial damage after coronary artery bypass grafting (CABG) is highly related to the methods used. Since indium-111 monoclonal antimyosin antibody scintigraphy has been shown to be highly specific and sensitive for myocardial necrosis, even in small lesions, uptake of this radiotracer was evaluated after CABG. In 23 consecutive patients without previous myocardial infarction who underwent CABG for stable angina, 80 MBq indium-111 antimyosin was injected on the third postoperative day. Planar images were obtained 48 hours later and analyzed for myocardial uptake of indium-111 antimyosin. Scintigraphic results were related to creatine kinase MB levels, duration of both aortic cross-clamping and cardiopulmonary bypass, and electrocardiographic changes. In all patients surgical procedure and postoperative course was uncomplicated. Indium-111 antimyosin uptake was present in 19 of 23 patients (82%). It was diffused in 7 patients and localized in 12. No pathologic Q waves occurred postoperatively. Fourteen patients exhibited ST-segment changes. No good relation was found among indium-111 antimyosin uptake and creatine kinase MB levels, duration of cross-clamping or bypass, and ST-T changes. It is concluded that some degree of myocardial damage, though silent, is common after CABG.

The role of prenylamine in the prevention of adriamycin-induced cardiotoxicity. A review of experimental and clinical findings.

Experimental and clinical trials to determine the potential of prenylamine in the prevention of adriamycin-related cardiotoxicity are reviewed. In mice given 4 mg/kg body weight adriamycin, the incidence of myocardial damage after 19 days' treatment was lower than in those given adriamycin and placebo. Rabbits were given adriamycin (total dose 10.8 mg/kg body weight), adriamycin plus prenylamine (1.5 mg/kg body weight), and adriamycin plus vitamins A (250 IU) and E (40 mg) for 9-11 weeks. Adriamycin-induced electrocardiogram changes were observed to a lesser extent in animals also receiving prenylamine. Heart homogenates from adriamycin-treated animals showed enhanced hydroperoxide-initiated chemiluminescence which was not affected by the simultaneous administration of prenylamine. The extent of adriamycin-induced myocytolysis and the degree of alterations observed on electron microscopy were markedly reduced by prenylamine. In a double-blind clinical trial with 26 oncological patients, no cardiomyopathy, arrhythmia or adverse reactions were observed in the group given adriamycin plus prenylamine. In those given adriamycin plus placebo, two patients developed congestive cardiopathy and another showed severe supraventricular arrhythmias together with hypotension and dyspnoea. The mechanisms of adriamycin-related cardiotoxicity, the effects of prenylamine and the benefit from combined treatment are discussed.