The missed diagnosis of aortic dissection in patients with acute myocardial infarction: a disastrous event.
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ABSTRACT:
SUBMITTER: Wang D
PROVIDER: S-EPMC5542992 | biostudies-other | 2017 Jul
REPOSITORIES: biostudies-other
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Project description:Acute aortic dissection (AAD) and acute myocardial infarction (AMI) are both severe cardiovascular diseases that may cause sudden death. However, whether serum proteins are differentially expressed between AAD and AMI remains unclear. Here, we aimed to explore serum protein profiles between AAD and AMI patients. A total of 75 serum samples were collected, including AAD patients without AMI (n = 25), AMI patients without AAD (n = 25), and normal subjects (n = 25). Protein identities and expression levels were assessed by LC-MS/MS analysis and a label-free quantitation method, respectively. After depletion of albumin and IgG, a total of 117 proteins with differential expression (fold change ≥2 or ≤−2.0, p < 0.05) were identified, of which 60 were upregulated and 57 were downregulated in AAD sera as compared to AMI sera. Bioinformatic analysis revealed that the differentially expressed serum proteins were mainly derived from exosomes and the extracellular space, and their molecular functions and biological processes were primarily involved in the activity of transporters and complements and the immune response. In addition, the serum level of Cadherin-5, an identified protein with significant regulation in AAD, was further evaluated by ELISA and the results showed that Cadherin-5 in AAD sera was higher that in AMI and healthy sera. Collectively, these findings reveal the differential serum protein profiles between AAD and AMI, which may reflect the divergent pathophysiological progression between the two cardiovascular diseases.
| S-EPMC9855332 | biostudies-literature
Project description:Background and Aims: The contradiction of management modality between acute myocardial infarction(AMI) and aortic dissection(AD) may result in clinical catastrophe. Data on risk factors, incidence, and outcome of AD and AMI are limited, and there have been no studies on the long-term outcomes of AMI in patients with AD. So we aimed to investigate long-term outcomes after AMI in patients with AD, and propose a useful diagnostic paradigm. Methods: Consecutively enrolled patients with AD and AMI who were referred to our center from 2010 to 2017. Baseline patient characteristics, risk factors, all medical treatments, echocardiographic parameters, laboratory data, and treatment were recorded. All patients were followed up from the first hospitalization until a first heart event, death, or 17 March, 2018. Results: 0.13% in AMI and 7.49% in AD patients had a concomitant diagnosis of AD and AMI. The average patient age was 53.3 ± 12.1 years and 84.6% were male. The most prevalent vascular risk factors were hypertension (69.2%) and current smoker (64.1%). Of all the 39 patients, 66.7% were managed surgically. Overall in-hospital mortality was 10.3%. The 30-day and 5-year fatality rates were 23.1% and 35.9%, but were higher for female than for male (66.7 vs. 30.3%, log-rank P = 0.045) on 5-year mortality. The overall survival of females was inferior to the males (log-rank P = 0.045). Conclusions: Patients with AMI and AD exhibit high 5-year fatality rates. For these patients, surgical management tends to have lower mortality. Improved management of hypertension and smoking, may reduce future incidence rates.
| S-EPMC8459711 | biostudies-literature
Project description:RATIONALE:Type A aortic dissection (TAAD) is a life-threatening disorder yet it is hard to diagnose. The dissection might extend to the coronary artery causing ST-segment elevation myocardial infarction (STEMI). Physicians might not recognize this particularly early in its presentation and patients proceed to receive the primary percutaneous coronary intervention. We present such a case and found that the marked pressure difference between the radial and ascending aortae could be a useful clue for diagnosing the aortic dissection-related myocardial infarction. PATIENT CONCERNS:A 58-year-old male was presented to our emergency department for the complaint of left side chest pain that lasted for an hour with concomitant hypotension. STEMI was diagnosed at that time. DIAGNOSIS:The emergent primary percutaneous intervention was performed. When the diagnostic catheter was advanced to the ascending aorta, the systolic aorta pressure became 20 mm Hg higher than radial systolic pressure. Due to the abnormally large pressure differential between the peripheral radial artery and central ascending aorta, TAAD was suspected. INTERVENTIONS:After angiography and computer tomography confirmed the diagnosis of TAAD, the patient was sent for emergent surgery. OUTCOMES:The patient was died because of extensive dissection and shock. LESSONS:We present such a case and found that the marked pressure difference between the radial and ascending aortae during catheterization could be a useful clue for diagnosing the aortic dissection-related myocardial infarction. This clue had hinted our speedy examination of the occluded coronary artery and dissection flap, and led to an early and accurate diagnosis.
| S-EPMC7220141 | biostudies-literature
Project description: Not available
| S-EPMC8343440 | biostudies-literature
Project description:BackgroundType A acute aortic dissection (AAD) is an extremely severe condition, having a high risk of mortality. Initial diagnosis can be deceptive, especially in patients with other confounding presentations.Case summaryWe present the case of a 60-year-old male with a history of endovascular aortic repair for abdominal aortic dissection, in whom a diagnosis of AAD was made, but almost missed, after he presented with stroke signs and left coronary myocardial infarction. Thorough clinical evaluation and point-of-care ultrasound (POCUS) were fundamental to the diagnosis of the underlying condition, which showed the intimal flap in the ascending aorta, aortic insufficiency, and a dissected left common carotid artery. The diagnosis was confirmed with a head and thoracic computed tomography scan, which also showed bilateral haemorrhagic strokes. Treatment options can be limited in patients with AAD with associated complications. After a careful multidisciplinary evaluation, life-sustaining therapy was withdrawn and the patient passed away.DiscussionOur case depicts the diagnosis challenge presented by patients with AAD. We emphasize the importance of clinical suspicion and POCUS examination for the diagnosis of the underlying condition, as it is frequently missed during first evaluation. We discuss the available literature regarding the prevalence and described mechanisms by which AAD can associate occlusion myocardial infarction, which more commonly involves the right coronary artery, as well as haemorrhagic stroke. We briefly mention management options, which are limited and controversial.
| S-EPMC10635585 | biostudies-literature
Project description:BackgroundPatients with atrial myocardial infarction (ATMI) have frequent cardiac and noncardiac complications. However, ATMI is uncommonly diagnosed because of its nonspecific ECG changes. Our objective was to analyze the ECG characteristics of ATMI in patients with inferior STEMI.HypothesisElectrocardiographic P wave parameters can help in diagnosis of ATMI.MethodsWe evaluated 932 patients who underwent coronary angiography and recruited 39 patients with ATMI and 33 patients without ATMI with inferior STEMI for a retrospective study. Twelve-lead ECGs were obtained to measure P-wave parameters in diagnosis of ATMI. P-wave parameters and PR-segment displacement were compared in patients with and without ATMI.ResultsIn inferior leads, PWD and PWDisp were significantly longer in the ATMI group than in the non-ATMI group (limb lead II, 109.79 ±15.51 ms and 86.65 ±5.02 ms, respectively; P < 0.001; limb lead III, 108.31 ±12.51 ms and 85.27 ±7.47 ms, P < 0.001; aVF, 106.49 ±13.68 ms and 83.01 ±7.89 ms, P < 0.001; PWDisp, 41.67 ±10.72 ms and 25.18 ±5.17 ms, P < 0.001). By contrast, PWA was significantly lower in the ATMI group than in the non-ATMI group (limb lead II, 0.96 ±0.18 mV and 1.39 ±0.22 mV, respectively; P < 0.001; limb lead III, 0.90 ±0.11 and 1.21 ±0.23, P < 0.001; aVF, 0.88 ±0.17 and 1.26 ±0.28, P < 0.001). PR-segment displacement was found in 8 (20.5%) patients with ATMI. A PWD ≥95.5 ms in lead DII diagnosed ATMI with a higher sensitivity and specificity (90%, 94%) than did PWA or PWDisp.ConclusionsThis study suggests P-wave parameters might be considered ECG findings in diagnosis of ATMI in patients with inferior STEMI.
| S-EPMC6489929 | biostudies-literature
Project description:Background: Aortic valve sclerosis (AVSc) presents similar pathogenetic mechanisms to coronary artery disease (CAD) and is associated with both short- and long-term mortality. In the context of acute myocardial infarction (AMI), evidence of specific systemic mechanisms characterizing AVSc are currently lacking. Objective: To evaluate the systemic pathophysiological landscape that might differentiate AVSc from non-AVSc subjects in AMI. Methods: Whole-blood transcriptome of AVSc (n=44) and no-AVSc (n=66) patients with AMI was assessed by RNA-sequencing. A bioinformatic workflow, including feature selection, differential expression and enrichment analysis was performed to identify gene expression signatures discriminating AVSc from no-AVSc and infer functional association. Multivariable Cox regression analysis was used to estimate hazard ratio of AVSc versus no-AVSc patients. Results: A signature of 100 informative genes allowed classifying AVSc from no-AVSc with 94% accuracy. Significant differences in 143 genes were also identified, 30 of which withstood association independently of age and previous AMI, or cardiac interventions. Functional inference unveiled significant association of AVSc with acute inflammatory and type I interferons (IFNs) response, platelet activation and hemostasis. AMI patients with AVSc showed a significantly higher incidence of adverse cardiovascular events within 10 years of follow-up with a full adjusted hazard ratio of 2.4 (95% CI 1.3–4.5). Conclusions: During AMI, AVSc patients showed increased type I IFNs response and associated adverse cardiovascular outcomes at follow-up. Novel pharmacological therapies aiming to inhibit response to type I IFNs during or immediately after AMI might improve poor cardiovascular outcomes of AMI patients with AVSc.
2024-01-31 | GSE218474 | GEO
Project description:Background Though rare, myocardial infarction secondary to coronary artery dissection is a life-threatening event. In reproductive age women, it commonly occurs during pregnancy or the postpartum period. Case We present a case of pregnancy-related acute myocardial infarction due to spontaneous coronary artery dissection in a 37-year-old woman who presented to the emergency room with shortness of breath and sudden onset of retrosternal chest pain 8 days after delivery of premature twins. Coronary artery catheterization showed 75 to 90% stenosis in the left main coronary artery (LMCA), extending into the proximal and mid left anterior descending (LAD) branch. The LMCA appearance in the heart catheterization was consistent with vasospasm, but it was not responsive to medical management. Subsequently, she underwent a second coronary artery catheterization and was found to have dissection requiring emergent coronary artery bypass graft × 3 in the LMCA, circumflex, and LAD that was followed by an uneventful recovery. Conclusion Early diagnosis and management of myocardial infarction due to coronary artery dissection in the peripartum period is crucial. This condition should be suspected in young reproductive age women, even in the setting of minimal risk factors. Angiography is required for diagnosis. Management should be individualized as it may include both invasive and noninvasive measures.
| S-EPMC4603869 | biostudies-other
Project description:Twenty-three AMI patients and 23 non-AMI healthy controls were included in this pilot study. Tissue samples were cut at 10 μm from formalin fixed paraffin-embedded tissue blocks using a microtome. Six to eight 10-μm sections were used for the isolation procedure. Total RNA isolation was performed using a miRNeasy FFPE kit (Qiagen) according to the manufacturer’s protocol. RNA concentration and purity was determined and before gene expression profiling (Affymetrix Human Exon 1.0ST Array). The microarray labeling, hybridization and processing was performed according to the manufacturer’s protocol at the Microarray Core Facility of Chinese National Human Genome Center, Shanghai, China. The raw data of microarray were quantile-normalized over all samples, summarized with the robust multi-array average (RMA) algorithm and log2 transformed with a median polish for ~22,000 transcript clusters (gene-level). Significance Analysis of Microarrays (SAM) was used to identify differential genes between AMI patients and non-AMI controls. Please note that the data files in this experiment have been previously submittted to NCBI Gene Expression Omnibus under accession numbers GSE38958 and GSE49081 (imported as E-GEOD-38958 and E-GEOD-49081 respectively in ArrayExpress ).
2016-05-11 | E-MTAB-3573 | biostudies-arrayexpress
Project description:BackgroundSpontaneous coronary artery dissection (SCAD) is an under-recognized acute cardiac disease entity. It is often missed, or misdiagnosed as coronary spasm, coronary atherosclerotic lesion, or thrombotic coronary occlusion. During the last years, SCAD also has been reported to be 'misdiagnosed as takotsubo syndrome (TS)' in patients with features consistent with both conditions. Spontaneous coronary artery dissection may present as an acute coronary syndrome and sometimes as sudden cardiac death.Case summaryWe report on the case of a 67-year-old woman who presented with features of ST-elevation myocardial infarction treated with fibrinolysis. The patient showed to have obtuse-marginal SCAD, which was misdiagnosed as fibrinolysis caused lysis of a coronary thrombus. The patient had moreover all other features of TS.DiscussionThis case report teaches important information about SCAD. The association between SCAD and TS are discussed.
| S-EPMC6426041 | biostudies-literature