Risk For In-hospital Cardiac Events Research Articles

PRE-EXISTING CARDIOVASCULAR DISEASE, ACUTE KIDNEY INJURY, AND CARDIOVASCULAR OUTCOMES IN HOSPITALIZED BLACKS WITH COVID-19 INFECTION

BACKGROUND: The Corona Virus 19 (COVID-19) infection is associated with worse outcomes in blacks, although the mechanisms are unclear. We sought to determine the significance of black race, pre-existing cardiovascular disease (pCVD), and acute kidney injury (AKI) on cardiopulmonary outcomes and in-hospital mortality of COVID-19 patients. METHODS: We conducted a retrospective cohort study of blacks with/without pCVD and with/without in-hospital AKI, hospitalized within Grady Memorial Hospital in Georgia between February and July 2020, who tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on qualitative polymerase-chain-reaction assay. The primary outcome was a composite of in-hospital cardiac events. RESULTS: Of the 293 patients hospitalized with COVID-19 in this study, 71 were excluded from the primary analysis (for race/ethnicity other than black non-Hispanic). Of the 222 hospitalized COVID-19 patients included in our analyses, 41.4% were female, 78.8% had pCVD, and 30.6% developed AKI during the admission. In multivariable analyses, pCVD (OR 4.7, 95% CI 1.5-14.8, P=0.008) and AKI (OR 2.7, 95% CI 1.3-5.5, P=0.006) were associated with increased odds of in-hospital cardiac events. AKI was associated with increased odds of in-hospital mortality (OR 8.9, 95% CI 3.3-23.9, P<0.0001). The presence of AKI was associated with increased odds of ICU stay, mechanical ventilation, and acute respiratory distress syndrome (ARDS). CONCLUSION: pCVD and AKI were associated with higher risk of in-hospital cardiac events, and AKI was associated with a higher risk of in-hospital mortality in blacks.

Racial differences in cardiopulmonary outcomes of hospitalized COVID-19 patients with acute kidney injury.

In-hospital acute kidney injury (IH-AKI) has been reported in a significant proportion of patients with COVID-19 and is associated with increased disease burden and poor outcomes. However, the mechanisms of injury are not fully understood. We sought to determine the significance of race on cardiopulmonary outcomes and in-hospital mortality of hospitalized COVID-19 patients with AKI. We conducted a retrospective cohort study of consecutive patients hospitalized in Grady Health System in Atlanta, Georgia between February and July 2020, who tested positive for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) on qualitative polymerase-chain-reaction assay. We evaluated the primary composite outcome of in-hospital cardiac events, and mortality in blacks with AKI versus non-blacks with AKI. In a subgroup analysis, we evaluated the impact of AKI in all blacks and in all non-blacks. Of 293 patients, effective sample size was 267 after all exclusion criteria were applied. The mean age was 61.4 ± 16.7, 39% were female, and 75 (28.1%) had IH-AKI. In multivariable analyses, blacks with IH-AKI were not more likely to have in-hospital cardiac events (aOR 0.3, 95% Confidence interval (CI) 0.04-1.86, p = 0.18), require ICU stay (aOR 0.80, 95% CI 0.20-3.25, p = 0.75), acute respiratory distress syndrome (aOR 0.77, 95% CI 0.16-3.65, p = 0.74), require mechanical ventilation (aOR 0.51, 95% CI 0.12-2.10, p = 0.35), and in-hospital mortality (aOR 1.40, 95% CI 0.26-7.50, p = 0.70) when compared to non-blacks with IH-AKI. Regardless of race, the presence of AKI was associated with worse outcomes. Black race is not associated with higher risk of in-hospital cardiac events and mortality in hospitalized COVID-19 patients who develop AKI. However, blacks with IH-AKI are more likely to have ARDS or die from any cause when compared to blacks without IH-AKI.

A new simple algorithm to stratify the risk of contrast-induced nephropathy in patients with acute coronary syndrome

Objectives and background: Previous studies on contrast-induced nephropathy (CIN) have identified contrast volume (CV) as a risk factor. The aim of our research was to define the safe dose of contrast media based on absolute CV, maximum allowable contrast dose (MACD) and estimated glomerular filtrate rate (eGFR). Methods and results: A total of 940 consecutive patients with acute coronary syndrome (ACS) were enrolled. Fifty-four patients developed CIN. MACD was defined as 5*body weight/serum creatinine. When using a CV higher than MACD, CIN-risk was increased 19-fold (OR 9.810—39.307, p<0.001). For the CV/eGFR ratio, we found that for every increase of one-tenth, CIN-risk increased by 4.9% (OR 1.037–1.061, p<0.001). The discriminative ability of CV (C statistic=0.626±0.038) was significantly lower than for the CV/MACD (C statistic=0.782±0.036, p=0.003) and CV/eGFR (C statistics: 0.796±0.033 for MDRD-4, 0.796±0.034 for Cockcroft-Gault, and 0.803±0.033 for CKD-EPI; p<0.001). There were no differences in the discriminative ability to predict CIN between the three eGFR equations. The combination of CV/MACD and CV/eGFR in a single protocol increases the positive predictive value of the Mehran risk score (40.7% vs 8.8%) with the same sensitivity (90.7% vs 83.3%). High doses of relative CV (CV/MACD and CV/eGFR) were also significantly associated with higher in-hospital mortality, reinfarction, and heart failure. ![Figure][1] Prediction of CIN risk Conclusions: A sequential protocol based on CV/MACD and CV/eGFR appropriately identified those ACS patients who developed CIN, with predictive values similar to a Mehran score, reducing the false positive rate. It is also useful to predict risk of in-hospital cardiac events regardless of GRACE score. [1]: pending:yes

Dosing of iodinated contrast volume: A new simple algorithm to stratify the risk of contrast‐induced nephropathy in patients with acute coronary syndrome

Previous studies on contrast-induced nephropathy (CIN) have identified contrast volume (CV) as a risk factor. The aim of our research was to define the safe dose of contrast media based on absolute CV, maximum allowable contrast dose (MACD) and estimated glomerular filtrate rate (eGFR). A total of 940 consecutive patients with acute coronary syndrome (ACS) were enrolled. Fifty-four patients developed CIN. MACD was defined as 5*body weight/serum creatinine. When using a CV higher than MACD, CIN-risk was increased 19-fold (OR 9.810-39.307, P < 0.001). For the CV/eGFR ratio, we found that for every increase of one-tenth, CIN-risk increased by 4.9% (OR 1.037-1.061, P < 0.001). The discriminative ability of CV (C statistic = 0.626 ± 0.038) was significantly lower than for the CV/MACD (C statistic = 0.782 ± 0.036, P = 0.003) and CV/eGFR (C statistics: 0.796 ± 0.033 for MDRD-4, 0.796 ± 0.034 for Cockcroft-Gault, and 0.803 ± 0.033 for CKD-EPI; P < 0.001). There were no differences in the discriminative ability to predict CIN between the three eGFR equations. The combination of CV/MACD and CV/eGFR in a single protocol increases the positive predictive value of the Mehran risk score (40.7% vs. 8.8%) with the same sensitivity (90.7% vs. 83.3%). High doses of relative CV (CV/MACD and CV/eGFR) were also significantly associated with higher in-hospital mortality, reinfarction, and heart failure. A sequential protocol based on CV/MACD and CV/eGFR appropriately identified those ACS patients who developed CIN, with predictive values similar to a Mehran score, reducing the false positive rate. It is also useful to predict risk of in-hospital cardiac events regardless of GRACE score.

Association of platelet‐monocyte aggregates with platelet activation, systemic inflammation, and myocardial injury in patients with non‐st elevation acute coronary syndromes

Platelet-monocyte aggregates (PMA) and C-reactive protein (CRP) are increased in unstable coronary disease. The interrelation of PMA with platelet activation, systemic inflammation, and their association with markers of myocardial injury has not been studied extensively. The study was undertaken to evaluate the association of CRP, PMA, and cardiac troponin I (cTnI) in patients admitted with non-ST elevation acute coronary syndromes (NSTE-ACS). In all, 69 consecutive patients with NSTE-ACS, 58 patients with stable angina pectoris (SAP), and 46 control patients without coronary artery disease were selected; PMA, sP-selectin, sCD40L inter leukin, (IL)-6, CRP, and cTnI concentrations were measured in these patients at the time of admission. Patients with NSTE-ACS were classified into two groups: those with troponin normal (cTnI < 0.06 ng/ml) and those with troponin elevation (cTnI > or = 0.06 ng/ml). Their risk for clinical in-hospital cardiac events (death and nonfatal myocardial infarction) was analyzed. Compared with SAP and control, patients with NSTE-ACS exhibited higher levels of PMA, sP-selectin, sCD40L, IL-6, and CRP. All these parameters were found to be higher (p < 0.001 ) in patients with troponin elevation than in those with normal troponin. There was a significant relationship between PMA and CRP (r =0.628, p < 0.001) and cTnI (r = 0.557, p < 0.001) in patients with NSTE-ACS. Logistic analysis further demonstrated that the presence of elevated PMA, CRP, and cTnI levels each confers and increases risk of future cardiac events. Levels of PMA and CRP were significantly increased in patients with NSTE-ACS, especially in those with troponin elevation. This increase is strongly related to the risk of in-hospital cardiac events. A panel of PMA, CRP, and cTnI may provide important information additional to current laboratory data for the treatment of NSTE-ACS.

High serum matrix metalloproteinase-9 level predict increased risk of in-hospital cardiac events in patients with type 2 diabetes and ST segment elevation myocardial infarction

IntroductionThe purpose of this study was to compare serum matrix metalloproteinase (MMP)-9 levels in a population of type 2 diabetic versus non-diabetic patients hospitalized with ST-segment elevation myocardial infarction (STEMI) and to examine the relationship between serum MMP-9 levels and the incidence of in-hospital cardiac events, including death and cardiogenic shock. MethodsWe recruited 120 patients with STEMI, of whom 48 were type 2 diabetic and 72 non-diabetic. Serum MMP-9 levels were measured on admission, using a commercially available ELISA. The primary study endpoint was cardiac death in-hospital and cardiogenic shock. ResultsMean serum MMP-9 levels were significantly higher in type 2 diabetic patients compared to non-diabetic patients (240±52ng/mL versus 185±47ng/mL; P<0.0001). In multivariable analysis, type 2 diabetes was an independent factor for mortality [OR: 1.75 (1.40–2.30); P=0.005] and cardiogenic shock [OR: 1.55 (1.20–1.70); P=0.03] when the variable MMP-9 level was not introduced into the model, but it was less significantly associated with mortality [OR: 1.60 (1.40–2.10); P=0.01] and no longer associated with cardiogenic shock when MMP-9 was in the model. ConclusionAfter STEMI, type 2 diabetes is independently associated with high serum MMP-9 levels. This elevated MMP-9 is strongly associated with the increased incidence of in-hospital mortality and cardiogenic shock observed in type 2 diabetes. Our findings clearly indicate that serum MMP-9 provides a highly valuable prognostic information on in-hospital outcome after STEMI, in particular in type 2 diabetic patients.

Tu-P7:270 High serum MMP-9 level found in diabetic patients after myocardial infarction is associated with an increased risk of in-hospital cardiac events

Tu-P7:270 High serum MMP-9 level found in diabetic patients after myocardial infarction is associated with an increased risk of in-hospital cardiac events

Myocardial global performance index as a predictor of in-hospital cardiac events in patients with first myocardial infarction

Objective We sought to assess the ability of a Doppler index of global myocardial performance (MPI), measured at entry, to predict inhospital cardiac events in a series of patients with first acute myocardial infarction (AMI). Methods A complete 2-dimensional and Doppler echocardiographic examination was performed within 24 hours of arrival at the coronary care department in 96 patients (81 men and 15 women; mean age 58 ± 9 years) with first AMI. Patients were divided a posteriori into 2 groups according to their inhospital course: group 1 comprised 75 patients with an uneventful course and group 2 comprised 21 patients with a complicated inhospital course (death, heart failure, arrhythmias, or post-AMI angina). Results There were no significant differences between the 2 groups with regard to history of hypertension, diabetes mellitus, hypercholesterolemia, site and size of infarction, and conventional parameters of diastolic function. However, patients with complications were significantly older (63 ± 10 vs 55 ± 8 years, P = .005) and had higher wall-motion score index and left ventricular end-systolic volume compared with patients without events (1.84 ± 0.27 vs 1.52 ± 0.30, P = .001; and 66 ± 29 vs 47 ± 21 mL, P = .009, respectively), whereas the ejection fraction was reduced (40 ± 10% vs 52 ± 10%, P = .0001). The mean value of the MPI was significantly higher in patients with cardiac events than in those without events (0.65 ± 0.20 vs 0.43 ± 0.16, P = .0001). A MPI ≥ 0.47 showed a sensitivity of 90% and specificity of 68% for identifying patients with events, on the basis of the receiver operator curve. In a multivariable model, the MPI at admission remained independently predictive of inhospital cardiac events (odds ratio 15.6, 95% confidence interval 2.4-99, P = .003). Conclusion These data suggest that in the acute phase of AMI, the MPI measured at entry may be useful to predict which patients are at high risk for inhospital cardiac events.

Dipyridamole echocardiographic test performed 3 days after an acute myocardial infarction: feasibility, tolerability, safety and in-hospital prognostic value.

In recent years, increasing evidence has pointed to the potential of dipyridamole stress echocardiography as a fast, effective, inexpensive method of risk stratification after an acute myocardial infarction. A very early stratification by this test could improve the patient's management and reduce the duration of in-hospital stay, and, thus, the costs. Two-hundred and fifty-one consecutive patients (208 male, age 58 +/- 11) with a two-dimensional echocardiogram of good technical quality underwent a dipyridamole echocardiographic test (DET) 70 +/- 6 h after an acute myocardial infarction. Criterion for positivity was the identification of a transient regional asynergy that was absent or of a lower degree in the baseline examination. Positivity was defined as 'at low-dose' or 'at high-dose' if the asynergy was detected before or after the 8th min of a drug infusion. All tests were performed without any major side effects. DET was positive in 149 (59%) and negative in 102 (41%) patients. During the hospital stay, cardiac events (death, reinfarction, angina) occurred in 52/251 patients: in 49/149 with a positive and in 3/102 with a negative test (sensitivity 94%, negative predictive value 97%, P < 0.00001). Severe events (death and reinfarction) occurred in 14/251: in 12/149 with a positive DET and in 2/102 with a negative DET (sensitivity 86%; negative predictive value: 98%; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Quantitative adenosine 201Tl single-photon emission computed tomography for the early assessment of patients surviving acute myocardial infarction.

We prospectively investigated whether adenosine 201Tl tomography (SPECT) could determine the extent of coronary artery disease, the presence of jeopardized myocardium, and the risk for in-hospital cardiac events in 120 clinically stable patients early (5 +/- 3 days) after myocardial infarction. All patients had coronary angiography and SPECT in close proximity. Adenosine SPECT identified 99% of infarct-related arteries and 82% of severely stenosed (> or = 70%) noninfarct arteries. Multivessel disease was accurately predicted in 69% of patients. Sixty-five percent of stenosed noninfarct arteries had matching thallium perfusion defects, and 92% of these were reversible. The specificity of adenosine SPECT was > 90%. Thallium redistribution occurred often within infarct (59%) and noninfarct (92%) zones. The patency status of the arteries, however, did not predict the presence or extent of jeopardized myocardium. The perfusion defect size was larger (p = 0.0001) in patients with (45 +/- 18%) than in those without (22 +/- 15%) in-hospital cardiac events. Furthermore, 90% of patients with events had a > or = 20% perfusion defect compared with only 38% of those without events (p = 0.0001). The positive-predictive accuracy for developing a cardiac event was 70% when the perfusion defect size was > 30%. The ischemic defect also was larger in patients with (19 +/- 14%) than in those without (10 +/- 10%) events (p = 0.001). The positive- and negative-predictive values for developing early postinfarction angina were 43% and 91%, respectively, when the ischemic defect was > 12%. In selected low-risk survivors of myocardial infarction, early quantitative adenosine SPECT is safe and accurate in detecting and localizing coronary stenoses, assessing the extent of jeopardized myocardium, and determining subsequent risk for in-hospital cardiac events.