Background: Depression has been suggested to increase the risk of cardiovascular disease, but many studies assessed depression after heart disease onset. This study evaluated the association between depression and myocardial infarction (MI) using a large inpatient database.Methods: We analyzed patients from the National Inpatient Sample hospitals from 2005 to 2020, selecting those aged >30 with ICD-9 and ICD-10 codes for segment elevation (ST) elevation myocardial infarction (STEMI), non-ST elevation myocardial elevation (NSTEMI) and major depression.Results: Our data included 4413,113 STEMI patients (224,430 with depression) and 10,421,346 NSTEMI patients (437,058 with depression). No significant association was found between depression and MI. For STEMI, the 2005 odds ratio was 0.12 (95% CI: 0.10-0.15, p < 0.001) and the 2020 odds ratio was 0.71 (95% CI: 0.69-0.73, p < 0.001). Similar patterns were observed for NSTEMI.Conclusion: Depression may not independently be a significant risk factor for MI.
Depression has been suggested to increase the risk of cardiovascular disease, but many studies assessed depression after heart disease onset. This study evaluated the association between depression and myocardial infarction (MI) using a large inpatient database. We analyzed patients from the National Inpatient Sample hospitals from 2005 to 2020, selecting those aged greater than 30. No significant association was found between depression and MI. Depression may not independently be a significant risk factor for MI. Our results suggest that patients with anxiety or depression have no association with the occurrence of MI.We suspect that the observed results may be related to the effects of selective serotonin reuptake inhibitors on platelets. Selective serotonin reuptake inhibitors primarily increase serotonin levels in the brain by inhibiting its reuptake. However, they can also affect platelet function by inhibiting serotonin reuptake by platelets. This inhibition of serotonin reuptake by platelets can lead to decreased platelet aggregation, which may confer some level of protection against certain conditions involving platelet dysfunction or excessive clotting. This effect is particularly relevant in cardiovascular diseases where abnormal platelet function can contribute to thrombotic events like heart attacks or strokes.

Cardiac amyloidosis is a rare but increasingly recognized condition characterized by the deposition of amyloid fibrils in cardiac tissue, leading to structural and functional heart impairment. This infiltrative cardiomyopathy often mimics more common cardiac conditions, posing significant diagnostic challenges. Particularly deceptive is its presentation as non-ST-segment elevation myocardial infarction (NSTEMI), where the clinical overlap necessitates considering amyloidosis in differential diagnoses. A 75-year-old male presented with muscle weakness, respiratory infection symptoms, and elevated cardiac enzymes. His history included a recent hospitalization for NSTEMI, with normal coronary angiography. Initial evaluations showed elevated troponin and CRP levels. A comprehensive cardiac assessment revealed a dilated ascending aorta, moderate systolic dysfunction (left ventricular ejection fraction (LV-EF), 47%), and asymmetrical interventricular septal thickening, suggesting hypertrophic cardiomyopathy or amyloidosis. The patient improved and was referred for further specialized care. Cardiac amyloidosis can mimic acute coronary syndrome (ACS), presenting with chest pain and elevated cardiac biomarkers. Differentiation is critical as amyloidosis involves myocardial infiltration by amyloid proteins, leading to restrictive cardiomyopathy. Advanced imaging techniques like cardiac MRI and nuclear scintigraphy are essential for accurate diagnosis and appropriate management, impacting therapeutic strategies and patient outcomes.

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With population aging and the subsequent accumulation of cardiovascular risk factors, a growing proportion of patients presenting with acute coronary syndrome (ACS) are octogenarian (aged between 80 and 89). The marked heterogeneity of this population is due to several factors like age, comorbidities, frailty, and other geriatric conditions. All these variables have a strong impact on outcomes. In addition, a high prevalence of multivessel disease, complex coronary anatomies, and peripheral arterial disease, increases the risk of invasive procedures in these patients. In advanced age, the type and duration of antithrombotic therapy need to be individualized according to bleeding risk. Although an invasive strategy for non-ST-segment elevation acute myocardial infarction (NSTEMI) is recommended for the general population, its need is not so clear in octogenarians. For instance, although frail patients could benefit from revascularization, their higher risk of complications might change the risk/benefit ratio. Age alone should not be the main factor to consider when deciding the type of strategy. The risk of futility needs to be taken into account and identification of risk factors for adverse outcomes, such as renal impairment, could help in the decision-making process. Finally, an initially selected conservative strategy should be open to a change to invasive management depending on the clinical course (recurrent angina, ventricular arrhythmias, heart failure). Further evidence, ideally from prospective randomized clinical trials is urgent, as the population keeps growing.

(1) Background: Due to similar clinical presentation and a lack of specific biomarkers, initial differentiation between Takotsubo syndrome (TTS) and non-ST-segment elevation myocardial infarction (NSTEMI) remains challenging in daily practice. Heat Shock Protein 70 (HSP70) is a novel biomarker that is recognized for its potential in the diagnosis and differentiation of cardiovascular conditions. (2) Methods: Data from a total of 156 patients were analyzed (32.1% NSTEMI, 32.7% TTS, and 35.3% controls). Serum concentrations of HSP70 were determined using ELISA and compared between patients and controls. ROC curve analysis, logistic regression analysis and propensity-score-weighted logistic regression were conducted. (3) Results: Concentrations of HSP70 were highest in patients with TTS (median 1727 pg/mL vs. ACS: median 1545 pg/mL vs. controls: median 583 pg/mL, p < 0.0001). HSP70 was predictive for TTS in binary logistic regression analysis (B(SE) = 0.634(0.22), p = 0.004), which even remained significant after correction for possible confounders in propensity-score-weighted analysis. ROC curve analysis also revealed a significant association of HSP70 with TTS (AUC: 0.633, p = 0.008). (4) Conclusions: Based on our findings, HSP70 constitutes a promising biomarker for discrimination between TTS and NSTEMI, especially in combination with established cardiovascular biomarkers like pBNP or high-sensitivity cardiac troponin.

BACKGROUND: PTSD leads to increased levels of stress hormones and dysregulation of the autonomic nervous system which may trigger cardiac events. The goal of this study is to evaluate any association between PTSD and the occurrence of STEMI and NSTEMI using a large database.
METHODS: Using the Nationwide Inpatient Sample (NIS) and ICD-9 codes from 2005 to 2014 (n=1,621,382), we performed a univariate chi-square analysis of in-hospital occurrence of STEMI and NSTEMI in patients greater than 40 years of age with and without PTSD. We also performed a multivariate analysis adjusting for baseline characteristics including age, gender, diabetes, race, hyperlipidemia, hypertension, and tobacco use.
RESULTS: The 2005-2014 dataset contained 401,485 STEMI patients (745, or 0.19%, with PTSD) and 1,219,897 NSTEMI patients (2,441, or 0.15%, with PTSD). In the 2005 dataset, 0.5% of PTSD patients had STEMI compared to 1.0% of non-PTSD patients (OR=0.46, 95% C.I., 0.36-0.59). Similarly, 0.6% of patients with PTSD and 2.2% of patients without PTSD had NSTEMI (OR=0.28, 95% C.I., 0.23-0.35). In the 2014 dataset, 0.3% of PTSD patients had STEMI compared to 0.7% of non-PTSD patients (OR=0.43, 95% C.I., 0.35-0.51). Similarly, 1.4% of patients with PTSD versus 2.9% of patients without PTSD had NSTEMI (OR=0.48, 95% C.I., 0.44-0.52). Similar trends were seen throughout the ten-year period. After adjusting for age, gender, diabetes, race, hyperlipidemia, hypertension, and tobacco use, PTSD was associated with a lower occurrence of STEMI (2005: OR=0.50, 95% C.I., 0.37-0.66; 2014: OR=0.35, 95% C.I., 0.29-0.43) and NSTEMI (2005: OR=0.44, 95% C.I., 0.34-0.57; 2014: OR=0.63, 95% C.I., 0.58-0.69).
CONCLUSIONS: Using a large inpatient database, we did not find an increased occurrence of STEMI or NSTEMI in patients diagnosed with PTSD, suggesting that PTSD is not an independent risk factor for myocardial infarction.

BACKGROUND: Biomarkers simplifying the diagnostic workup by discriminating between non-ST-segment-elevation myocardial infarction (NSTEMI) and infarct-like myocarditis are an unmet clinical need.
RESULTS: A total of 105 subjects were categorized into groups as follows: ST-segment-elevation myocardial infarction (n=36), NSTEMI (n=22), infarct-like myocarditis (n=19), cardiomyopathy-like myocarditis (n=18), and healthy control (n=10). All subjects underwent cardiac magnetic resonance imaging, and serum concentrations of matrix metalloproteinase-1 (MMP-1) and procollagen type I carboxy terminal propeptide (PICP) were measured. Biomarker concentrations in subjects presenting with acute coronary syndrome and non-ST-segment-elevation, for example NSTEMI or infarct-like myocarditis, categorized as the non-ST-segment-elevation acute coronary syndrome-like cohort, were of particular interest for this study. Compared with healthy controls, subjects with myocarditis had higher serum concentrations of MMP-1 and PICP, while no difference was observed in individuals with myocardial infarction. In the non-ST-segment-elevation acute coronary syndrome-like cohort, MMP-1 concentrations discriminated infarct-like myocarditis and NSTEMI with an area under the receiver operating characteristic curve (AUC) of 0.95 (95% CI, 0.89-1.00), whereas high-sensitivity cardiac troponin T performed inferiorly (AUC, 0.74 [95% CI, 0.58-0.90]; P=0.012). Application of an optimal MMP-1 cutoff had 94.4% sensitivity (95% CI, 72.7%-99.9%) and 90.9% specificity (95% CI, 70.8%-98.9%) for the diagnosis of infarct-like myocarditis in this cohort. The AUC of PICP in this context was 0.82 (95% CI, 0.68-0.97). As assessed by likelihood ratio tests, incorporating MMP-1 or PICP with age and C-reactive protein into composite prediction models enhanced their diagnostic performance.
CONCLUSIONS: MMP-1 and PICP could potentially be useful biomarkers for differentiating between NSTEMI and infarct-like myocarditis in individuals with non-ST-segment-elevation acute coronary syndrome-like presentation, though further research is needed to validate their clinical applicability.

Non-ST segment elevation myocardial infarction (NSTEMI) is a relatively unknown complication of injecting sublingual Suboxone (buprenorphine/naloxone). Buprenorphine/naloxone should be taken as a sublingual tablet or a buccal film and not injected, so its effects from this mode of administration are not well known. While the differential diagnosis for chest pain is very broad, many practitioners do not associate chest pain with the use of buprenorphine/naloxone. We recommend considering serial electrocardiograms (ECGs) and high-sensitivity troponins for a patient who presents with chest pain after buprenorphine/naloxone use.

BACKGROUND: In suspected non-ST-segment elevation myocardial infarction (NSTEMI), this presumed diagnosis may not hold true in all cases, particularly in patients with nonobstructive coronary arteries (NOCA). Additionally, in multivessel coronary artery disease, the presumed infarct-related artery may be incorrect.
OBJECTIVE: This study sought to assess the diagnostic utility of cardiac magnetic resonance (CMR) before invasive coronary angiogram (ICA) in suspected NSTEMI.
METHODS: A total of 100 consecutive stable patients with suspected acute NSTEMI (70% male, age 62 ± 11 years) prospectively underwent CMR pre-ICA to assess cardiac function (cine), edema (T2-weighted imaging, T1 mapping), and necrosis/scar (late gadolinium enhancement). CMR images were interpreted blinded to ICA findings. The clinical care and ICA teams were blinded to CMR findings until post-ICA.
RESULTS: Early CMR (median 33 hours postadmission and 4 hours pre-ICA) confirmed only 52% (52 of 100) of patients had subendocardial infarction, 15% transmural infarction, 18% nonischemic pathologies (myocarditis, Takotsubo and other forms of cardiomyopathies), and 11% normal CMR; 4% were nondiagnostic. Subanalyses according to ICA findings showed that, in patients with obstructive coronary artery disease (73 of 100), CMR confirmed only 84% (61 of 73) had MI, 10% (7 of 73) nonischemic pathologies, and 5% (4 of 73) normal. In patients with NOCA (27 of 100), CMR found MI in only 22% (6 of 27 true MI with NOCA), and reclassified the presumed diagnosis of NSTEMI in 67% (18 of 27: 11 nonischemic pathologies, 7 normal). In patients with CMR-MI and obstructive coronary artery disease (61 of 100), CMR identified a different infarct-related artery in 11% (7 of 61).
CONCLUSIONS: In patients presenting with suspected NSTEMI, a CMR-first strategy identified MI in 67%, nonischemic pathologies in 18%, and normal findings in 11%. Accordingly, CMR has the potential to affect at least 50% of all patients by reclassifying their diagnosis or altering their potential management.

UNASSIGNED: Infective endocarditis (IE) is a rare disease associated with high mortality rates. Clinical presentation is highly variable with a time interval between first onset of symptoms and diagnosis > 1 month in 25% of patients. We present a case of aortic valve endocarditis with aortic root abscess (ARA) with chest pain and ischaemic changes on the electrocardiogram (ECG).
UNASSIGNED: A 59-year-old Caucasian male with a known bicuspid aortic valve presented at our emergency department with a 2-week history of malaise, subfebrile temperatures, and chest pain episodes. The ECG exhibited ischaemic changes, and laboratory workup showed elevated inflammatory markers and troponin levels. Coronary angiography revealed a one-vessel coronary artery disease with a borderline significant stenosis of the left circumflex artery. Cardiac magnetic resonance imaging showed a large aortic valve vegetation with an ARA expanding intramyocardially, which was not seen on bedside echocardiography. The patient was set on intravenous (i.v.) antibiotics and urgently referred for surgery. The patient received surgical aortic root and valve replacements, reconstruction of the anterior mitral leaflet, and a venous bypass. After successful surgical management followed by 6 weeks of i.v. antibiotics, the patient completely recovered.
UNASSIGNED: Diagnosing IE in atypical cases, such as those with ischaemic ECG changes, remains challenging. Infective endocarditis should be considered as an early differential diagnosis in individuals with prosthetic or native valve disease. Infective endocarditis poses a significant risk for perivalvular and ARA formation with high mortality. Aortic root abscess may present with unspecific symptoms or unusual ECG changes and might be missed in standard transthoracic echocardiography in up to 30% of cases. Multimodal imaging can help in establishing a prompt and accurate diagnosis, aid in timely treatment and mitigating the risk of complications of IE.