Spontaneous coronary artery dissection (SCAD) is a nonatherosclerotic, noniatrogenic cause of acute coronary syndrome (ACS) that predominantly affects women, including those of reproductive age. Misdiagnosis as atherosclerotic coronary disease may lead to inappropriate interventions and antithrombotic therapy. This narrative review summarizes consensus statements, registry data, and observational studies published through July 2026 to provide a structured, clinically oriented overview of the diagnosis, acute management, and long-term care of SCAD. Most recommendations are based on observational studies or registry-level evidence; randomized trial data remain limited. A narrative review of the literature was performed using MEDLINE/PubMed, EMBASE, and the Cochrane Library. Search terms included "spontaneous coronary artery dissection," "SCAD," "fibromuscular dysplasia," "intramural hematoma," and related terms. The search was not date-restricted but was updated through July 2026. Priority was given to guideline documents, consensus statements, registries, systematic reviews, and original cohort studies. The review highlights the angiographic recognition of SCAD patterns and the selective use of intravascular imaging in ambiguous cases. A conservative management strategy is preferred in hemodynamically stable patients with preserved distal coronary flow and no objective evidence of ongoing ischemia, given the high rates of spontaneous healing and the risk of iatrogenic dissection. Revascularization may be considered in selected high-risk patients with ongoing ischemia or hemodynamic compromise. Long-term care includes individualized antiplatelet therapy, beta-blockers, extracoronary arteriopathy screening, rehabilitation, and counseling regarding pregnancy and trigger avoidance. This review provides a clinically applicable framework for SCAD diagnosis and management while highlighting persistent evidence gaps in antithrombotic strategies, recurrence prediction, and extracoronary screening.
Spontaneous coronary artery dissection (SCAD) is an important cause of acute myocardial infarction in women without significant atherosclerotic coronary artery disease. Recurrent SCAD progressing to advanced heart failure requiring durable mechanical circulatory support is exceptionally uncommon. A 45-year-old woman with a mechanical mitral valve prosthesis presented with non-ST-segment elevation myocardial infarction caused by multivessel SCAD involving the circumflex artery (Type 1) and the first obtuse marginal branch (OM1) (Type 2A). Because coronary flow was preserved (TIMI 3), conservative management was adopted. Follow-up angiography demonstrated healing of the OM1 lesion and a stable residual circumflex dissection. Two years later, she presented with anterior ST-segment elevation myocardial infarction. Coronary angiography demonstrated an abrupt, near-total occlusion of the left anterior descending artery, which was considered most compatible with recurrent Type 4 SCAD after alternative diagnoses, including coronary thromboembolism, were excluded. Despite intracoronary vasodilator therapy, persistent ischemia necessitated percutaneous coronary intervention with drug-eluting stent implantation, restoring TIMI 3 flow. Severe left ventricular systolic dysfunction developed despite successful revascularization and optimal medical therapy. During follow-up, the patient underwent implantation of an implantable cardioverter-defibrillator (ICD) for primary prevention and, after recurrent heart failure hospitalizations over 18 months, durable left ventricular assist device (LVAD) implantation as a bridge to heart transplantation. This case demonstrates that angiographic healing after conservatively managed SCAD does not eliminate the risk of recurrence in previously unaffected coronary territories. It underscores the diagnostic challenges of Type 4 SCAD in patients with competing causes of myocardial infarction and illustrates that recurrent SCAD may rarely progress to advanced heart failure requiring durable mechanical circulatory support.
OBJECTIVE:This study aimed to evaluate age-related differences in the clinical, inflammatory, and angiographic characteristics of patients with myocardial infarction (MI). METHOD:This retrospective, single-center observational study analyzed 905 consecutive patients with acute MI who underwent coronary angiography between February 2024 and April 2026. Patients were divided into three age groups: <45 years (n=96), 45-54 years (n=226), and ≥55 years (n=583). Demographic characteristics, cardiovascular risk factors, inflammatory indices, laboratory findings, and angiographic features were retrospectively analyzed. RESULTS:The mean age was 61.0+-13 years, and 71.2% of the patients were male. ST-segment elevation myocardial infarction was present in 59.4% of young patients. Young patients had a higher prevalence of ever smoking, higher admission low-density lipoprotein cholesterol levels, a higher prevalence of high TIMI thrombus burden, and more frequent bifurcation lesions. In contrast, hypertension, diabetes mellitus, chronic kidney disease, and previous coronary artery disease were less common among young patients. Exploratory multinomial logistic regression analyses identified fewer statistically significant adjusted associations when comparing patients aged 45-54 years with those aged <45 years than when comparing patients aged ≥55 years with those aged <45 years. CONCLUSION:Age-related differences were observed in the clinical, inflammatory, and angiographic characteristics of patients with MI, with fewer between-group differences between young and middle-aged patients than between young and older patients. These findings represent descriptive associations derived from a retrospective, single-center observational study and should not be interpreted as causal.
Electrical injury may cause various cardiac complications, including electrocardiographic (ECG) changes that mimic acute myocardial infarction. We present a 38-year-old man who developed cardiopulmonary arrest after exposure to a 25,000-volt electrical current. The admission ECG showed inferolateral ST-segment elevation, raising suspicion for acute myocardial infarction. Cardiac biomarkers were markedly elevated, and transthoracic echocardiography demonstrated a left ventricular ejection fraction (LVEF) of 35% with inferoposterolateral wall hypokinesia accompanied by moderate mitral regurgitation. Emergency coronary angiography demonstrated no significant obstructive coronary artery disease. The post-coronary angiography ECG showed greater than 50% resolution of the ST-segment elevation. A 24-hour follow-up ECG demonstrated near-complete resolution of the ST-segment abnormalities, while repeat echocardiography showed complete recovery of left ventricular systolic function, resolution of the previously detected regional wall motion abnormalities, and regression of mitral regurgitation to a trivial degree. Although ventricular function normalized within 24 hours, the patient subsequently developed dialysis-requiring acute kidney injury, neurological deterioration, suspected pneumonia, and refractory septic shock and died on hospital day 10. This case highlights that high-voltage electrical injury may present with ST-segment elevation despite the absence of obstructive coronary artery disease, accompanied by reversible myocardial dysfunction, emphasizing the importance of considering ST-segment elevation myocardial infarction (STEMI) mimics in the differential diagnosis.
OBJECTIVE:Acute kidney injury may complicate acute myocardial infarction and has prognostic significance in broad acute coronary syndrome cohorts. However, the timing of early kidney injury and the prognostic differentiation among acute kidney injury phenotypes remain insufficiently characterized in critically ill patients with acute myocardial infarction who meet premature-age criteria and require intensive care. METHOD:This retrospective cohort study used MIMIC-IV, a deidentified, single-center critical care database from an academic health system in the United States. The study cohort should be interpreted as ICU-admitted patients with AMI codes who met prespecified sex-specific premature-age criteria rather than as a general young or angiographically adjudicated premature myocardial infarction population. Premature myocardial infarction was prespecified as age younger than 55 years in men and younger than 65 years in women. The primary exposure was early creatinine-defined acute kidney injury reconstructed according to the KDIGO serum creatinine relative and absolute change criteria, with the first qualifying creatinine-based onset occurring within 0-48 hours after ICU admission. Urine-output and renal-replacement-therapy variables were derived separately for phenotype analyses and were not incorporated into the primary exposure. The primary outcome was 1-year all-cause mortality. The main analysis used a time-dependent Cox model, with landmark phenotype analyses performed as supportive analyses. RESULTS:The cohort included 1261 patients, of whom 363 (28.8%) developed early creatinine-defined acute kidney injury. Within 1 year, 275 patients died (21.8%), including 151 deaths during the index hospitalization (12.0%). Early creatinine-defined acute kidney injury was associated with higher mortality in the primary time-dependent Cox model (hazard ratio 1.37, 95% confidence interval 1.06-1.79; P=0.018). The association was also maintained in the supportive parsimonious multivariable Cox model (hazard ratio 1.63, 95% confidence interval 1.23-2.16; P<0.001). The expanded complete-case model and prespecified multiple-imputation sensitivity analysis also supported an association in the same direction. In the 24-hour landmark analysis, the urine-output-only acute kidney injury phenotype did not retain an independent association with mortality, whereas the creatinine- or renal-replacement-therapy-positive phenotype remained directionally associated with higher risk. CONCLUSION:Early creatinine-defined acute kidney injury may serve as a marker of increased risk among ICU-admitted, AMI-coded patients who meet sex-specific premature-age criteria. The findings should not be generalized to all young or premature myocardial infarction patients and should be interpreted cautiously in view of ICU-only selection, coding-based disease definitions, incomplete etiologic profiling, and residual confounding.
OBJECTIVE:This study aimed to determine the demographic and clinical profiles, cardiovascular risk factors, and variables independently associated with major adverse cardiovascular events (MACE) during 1-year follow-up in young patients aged 45 years or younger who presented with suspected ST-segment elevation myocardial infarction (STEMI) and underwent emergency coronary angiography. METHOD:This retrospective, single-center, observational study included 126 young patients presenting with suspected STEMI who underwent primary coronary angiography and/or percutaneous coronary intervention at a high-volume tertiary cardiovascular center between January 2021 and April 2025. Patients were classified into two groups according to the occurrence of MACE during 1-year follow-up: the MACE group (n=28) and the non-MACE group (n=98). HbA1c levels were assessed based on a single measurement obtained during the index MI admission. Logistic regression analyses were performed to identify variables independently associated with MACE. RESULTS:The median age of the overall cohort was 40 years (38-42), and 7.9% of the patients were female. During follow-up, MACE occurred in 22.2% of the patients. The all-cause mortality rate was 4.0%. Multivariable logistic regression analysis demonstrated that higher HbA1c levels (aOR: 1.57; 95% CI: 1.10-2.24; P = 0.014), a history of CAD (aOR: 3.93; 95% CI: 1.15-13.37; P = 0.029), and lower LVEF (aOR: 0.94; 95% CI: 0.88-0.99; P = 0.029) were independently associated with MACE. Notably, among patients without previously known diabetes, HbA1c levels ≥6.5% were significantly associated with an increased risk of MACE. CONCLUSION:Young patients presenting with suspected STEMI who undergo emergency coronary angiography may have a notable risk of MACE during the first year of follow-up. A history of CAD, lower LVEF, and elevated HbA1c levels appear to be associated with adverse clinical outcomes.
OBJECTIVE:Current clinical guidelines for non-ST-segment elevation myocardial infarction (NSTEMI) emphasize the duration of dual antiplatelet therapy (DAPT) based on scores such as the Predicting Bleeding Complications in Patients Undergoing Stent Implantation and Subsequent Dual Antiplatelet Therapy (PRECISE-DAPT) score and the Dual Antiplatelet Therapy (DAPT) score. However, these anatomical and clinical models often overlook the "inflammatory gap,' namely the contribution of systemic inflammation to both thrombotic and hemorrhagic risk. Although traditional models focus primarily on anatomical complexity, systemic inflammation may serve as a silent driver of adverse outcomes. We aimed to evaluate, using an artificial intelligence (AI)-enhanced approach, the incremental prognostic value of the inflammation-based Modified Glasgow Prognostic Score (mGPS) over a 36-month follow-up period, with particular emphasis on capturing non-linear interactions between biological markers and long-term outcomes. METHOD:This study included 456 NSTEMI patients who underwent percutaneous coronary intervention (PCI). mGPS, DAPT, and PRECISE-DAPT scores were calculated for all patients. Prognostic performance was assessed using a Gradient Boosting Machine (GBM)-based machine learning (ML) framework. Analyses focused on improvements in the concordance index (C-index), Net Reclassification Index (NRI), and Integrated Discrimination Improvement (IDI), as well as three-year mortality assessed using Cox proportional hazards modeling to identify residual inflammatory risk. Model calibration was evaluated using the Brier score. RESULTS:At 36 months, mGPS emerged as the strongest independent predictor of mortality. Compared with patients with mGPS 0, those with mGPS 2 demonstrated a 6.18-fold higher risk of mortality (hazard ratio 6.18; 95% confidence interval 2.95-12.94; P < 0.001). Observed mortality rates increased markedly from 3.2% in the mGPS 0 group to 57.1% in the mGPS 2 group (P < 0.001). While mGPS was not significantly associated with the ischemic DAPT score (P = 0.349), it was strongly associated with high bleeding risk (PRECISE-DAPT ≥ 25), with all patients in the mGPS 2 category classified as high bleeding risk (P < 0.001). Incorporation of mGPS into the baseline AI model significantly improved discriminative performance, increasing the C-index from 0.72 to 0.81 (P = 0.008). Additionally, the model correctly reclassified 46% of patients (NRI 0.46, P < 0.001) and demonstrated significant predictive improvement (IDI 0.08, P = 0.004) compared with traditional scoring systems. CONCLUSION:Systemic inflammation, as quantified by mGPS, is a critical biological modifier of cardiovascular risk that may help bridge the "inflammatory gap" in current scoring systems. AI-driven integration of mGPS into conventional clinical scores significantly improves 36-month prognostic reclassification. mGPS appears to function as a biological recalibrator, identifying high-risk individuals who may be misclassified by conventional scoring systems. These findings suggest that mGPS-guided personalized antiplatelet strategies-particularly early DAPT de-escalation in patients with elevated mGPS-may help reduce the high mortality and bleeding risk observed in this vulnerable population by addressing biological fragility in addition to anatomical risk.
OBJECTIVE:Mitral balloon valvuloplasty remains an established first-line treatment for appropriately selected patients with rheumatic mitral stenosis. However, predictors of long-term restenosis and the additional value of periinterventional transesophageal echocardiography remain incompletely defined. METHOD:This retrospective, single-center study included 555 patients who underwent percutaneous mitral balloon valvuloplasty for rheumatic mitral stenosis between January 2010 and January 2025 at Mehmet Akif Ersoy Heart Center, İstanbul, Türkiye. Patients were divided according to the presence or absence of restenosis at the 1-year follow-up. Restenosis was defined as a mitral valve area <1.5 cm². Procedural success was defined as less than moderate mitral regurgitation at the end of the procedure and the absence of transseptal puncture-related complications. Clinical, echocardiographic, procedural, and laboratory variables were analyzed to identify predictors of restenosis and procedural success. RESULTS:Restenosis occurred in 94 patients (17%). The mean age of the overall cohort was 47.81+-12.29 years, and 467 patients (84.1%) were female. Patients with restenosis had higher preprocedural systolic pulmonary artery pressure, postprocedural transmitral gradient, postprocedural systolic pulmonary artery pressure, and preprocedural Wilkins score. In multivariable analysis, only the preprocedural Wilkins score remained an independent predictor of restenosis (OR: 1.907, 95% CI: 1.339-2.718, P < 0.001). Post-balloon transmitral gradient and postprocedural left atrial pressure ≥12 mmHg were associated with procedural success. Periinterventional transesophageal echocardiography was not associated with restenosis or procedural success. CONCLUSION:In patients undergoing percutaneous mitral balloon valvuloplasty for rheumatic mitral stenosis, the preprocedural Wilkins score was the only independent predictor of 1-year restenosis. Routine periinterventional transesophageal echocardiography did not significantly influence procedural success or long-term restenosis rates. These findings suggest that, in appropriately selected patients, percutaneous mitral balloon valvuloplasty can be safely and effectively performed under transthoracic echocardiographic guidance without routine periinterventional transesophageal echocardiography.
Late stent thrombosis is an uncommon but potentially fatal complication following percutaneous coronary intervention. In young patients presenting with recurrent myocardial infarction despite appropriate secondary prevention, underlying prothrombotic disorders should be considered. A 39-year-old man presented with out-of-hospital cardiac arrest nine months after implantation of a 2.75×28 mm drug-eluting stent in the left anterior descending artery for anterior ST-segment elevation myocardial infarction. Coronary angiography demonstrated late thrombotic occlusion of the previously implanted stent with TIMI 0 flow. Successful balloon angioplasty followed by kissing balloon inflation restored TIMI 3 flow in both the left anterior descending artery and the diagonal branch. Because of recurrent myocardial infarction due to late stent thrombosis at a young age, the presence of limited conventional risk factors sufficient to explain the clinical presentation, and no reported history of nonadherence to medical therapy, a systematic laboratory evaluation for thrombophilia and antiphospholipid syndrome was performed. Persistent lupus anticoagulant positivity was demonstrated on repeated testing, whereas anticardiolipin and anti-β2-glycoprotein I antibodies were negative. Following multidisciplinary evaluation by the Departments of Cardiology and Rheumatology, the findings supported a clinical diagnosis of primary antiphospholipid syndrome. Long-term vitamin K antagonist therapy was recommended but declined by the patient. At the four-month follow-up after implantable cardioverter-defibrillator implantation, no recurrent thrombotic events or ICD therapies were observed. Young patients presenting with recurrent myocardial infarction secondary to late stent thrombosis, particularly in the absence of documented interruption of dual antiplatelet therapy, should be considered for systematic evaluation of thrombophilic disorders, including antiphospholipid syndrome.
OBJECTIVE:To characterize adults younger than 45 years with myocardial infarction (MI) and examine factors associated with multivessel disease. METHOD:This single-center retrospective study included patients aged 18-44 years who were hospitalized between January 2024 and January 2026 with STEMI, NSTEMI, or a working diagnosis of MI with nonobstructive coronary arteries (MINOCA). Patients with alternative diagnoses or type 2 MI were excluded. Logistic regression analysis was performed among patients with obstructive coronary disease. RESULTS:Among 180 patients, the mean age was 39.0+-4.1 years, and 160 (88.9%) were male. Low sex-specific HDL-C levels were present in 78.9%, triglyceride levels ≥150 mg/dL in 56.4%, LDL-C levels ≥130 mg/dL in 44.5%, and LDL-C levels ≥160 mg/dL in 22.0%. Multivessel disease was present in 65 of 164 patients with obstructive disease (39.6%). In the exploratory primary model, each 5-mg/dL decrease in HDL-C was associated with multivessel disease (adjusted odds ratio, 1.35; 95% confidence interval, 1.02-1.77; P = 0.034). In a separately specified alternative model using non-HDL-C as the sole lipid covariate, the adjusted association estimate for non-HDL-C did not reach statistical significance (adjusted odds ratio, 1.13 per 25-mg/dL increase; 95% confidence interval, 0.95-1.35; P = 0.175). The composite in-hospital adverse event occurred in 14 patients (7.8%), and mortality was 1.1%. CONCLUSION:In the exploratory primary model, lower HDL-C levels were associated with multivessel disease. In a separately specified alternative model, the adjusted association estimate for non-HDL-C did not reach statistical significance. Because the models differed in covariate composition and complete-case populations and were not designed for direct comparison, these findings do not establish the relative importance of HDL-C and non-HDL-C.
OBJECTIVE:Repeat revascularization following percutaneous coronary intervention (PCI) remains an important clinical concern in young patients. We evaluated the clinical and atherogenic factors associated with repeat revascularization in patients with premature non-ST-segment elevation myocardial infarction (NSTEMI) undergoing PCI. METHOD:This retrospective, single-center observational study included 466 consecutive patients younger than 45 years who underwent PCI for NSTEMI between January 2020 and December 2024. Atherogenic markers, including the atherogenic index of plasma (AIP), triglyceride-glucose (TyG) index, remnant cholesterol inflammation index (RCII), and Castelli risk indices I and II (CRI-I and CRI-II), were analyzed. The primary endpoint was repeat revascularization only. A nested multivariable Cox model was used to evaluate the incremental prognostic value of CRI-II beyond that of a baseline model. RESULTS:Repeat revascularization occurred in 73 individuals (16%) over a median follow-up of 37.2 (22.1-51.9) months, predominantly involving non-target vessel revascularization. Patients requiring repeat revascularization had significantly higher CRI-II levels (P = 0.03). CRI-II remained independently associated with repeat revascularization after adjustment, along with hypertension and bifurcation lesions (HR: 1.30, 95% CI: 1.09-1.55, P = 0.003; HR: 2.09, 95% CI: 1.27-3.45, P = 0.004; and HR: 2.26, 95% CI: 1.19-4.27, P = 0.01, respectively); the addition of CRI-II modestly improved discrimination (Harrell's C index: 0.684 to 0.694). High CRI-II was associated with significantly higher repeat revascularization rates in the Kaplan-Meier analysis (log-rank P < 0.0001). CONCLUSION:Elevated CRI-II was independently associated with repeat revascularization, along with hypertension and bifurcation lesions, in patients with premature NSTEMI undergoing PCI. However, CRI-II showed limited discriminatory performance, and its clinical utility for risk stratification requires external validation.
