European Journal of Cardiovascular Medicine

Acute Myocardial Infarction (AMI) is a leading cause of morbidity and mortality worldwide, despite substantial improvements in prognosis over the past decade (1). AMI can be divided into 2 categories: non–ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI). Unstable angina resembles an NSTEMI, but normal cardiac markers distinguish it (2)(3). Although the risk of suffering an AMI increases with older age (4), the incidence of AMI in younger patients (<45 years of age) has progressively increased over time (5).

Premature atherosclerosis with plaque rupture or plaque erosion is the most common etiology, accounting for almost 90% of AMI in young adults. The remaining 10% of cases are secondary to nonplaque etiologies that include spontaneous coronary artery dissection (SCAD), coronary vasospasm, hypercoagulability, coronary embolic phenomena, autoimmune‐mediated inflammation, and drug‐induced occlusions (5).

Here we report a case of young female who presented with Acute myocardial Infarction (STEMI) post Dilatation and curettage (D&C). and plaque rupture was suspected as cause of STEMI post D&C.

A 38-year-old female presented in cardiology emergency with complaints of severe chest pain for last six hours, radiating to left upper limb and associated with sweating. She had undergone Dilatation & Curettage for her miscarriage the same day at a peripheral centre. She had no past medical history and no known risk factor for cardiovascular disease. Her family history was unremarkable.

On Examination, her consciousness appeared clear with GCS score of 15 (E4V5M6). Her BP and pulse rate was 144/80 mmhg and 76 beats/min respectively. The BMI was 24.2 kg/m², body temperature was 36.5 °C, Respiratory rate 16/min and oxygen saturation was 99% on room air. The routine laboratory investigations were normal. Her Troponin T (qualitative) was positive at the time of presentation.

A 12 lead ECG showed ST elevation in lead V1, V2, V3, V4, V5, V6 with reciprocal depression in lead III and aVF. [image-1] A transthoracic echocardiography confirmed hypokinesia of apical septum, apex and apical lateral segments with left ventricular ejection fraction of 35-40%. [image- 2a, 2b, 2c] However, other Echo parameters were normal. She was preloaded with 300 mg Aspirin, 180 mg Ticagrelor and 80 mg Atorvastatin.

Image- 1- A 12 lead ECG showing ST elevation in V1-V6 with reciprocal ST depression in lead III and avf

Transthoracic Echo showing hypokinesia of apical septum, apex and apical anterolateral segments in 4 chamber (2a), parasternal short axis (2b) and parasternal long axis view (2c)

On the basis of symptoms, ECG and Echo reports, provisional diagnosis of Anterior wall STEMI was made and patient was taken for urgent coronary angiogram. Coronary angiogram was carried out using the right radial artery with 6 Fr sheath and it revealed 100% occlusion of mid left anterior descending (LAD). In addition, no abnormal findings such as coronary artery aneurysm and spontaneous coronary artery dissection (SCAD) was present. Optical coherence tomography (OCT) was done to know about the plaque morphology and etiology, it was suggestive of plaque rupture. [image-3]

image- 3 OCT pullback showing plaque rupture with red thrombus

Coronary angiography from right radial route showing grade III thrombus in mid LAD with significant stenosis (4a), Post thrombo-suction (4b) , Post dilatation and stenting with drug eluting stent (4c)

In view of the above findings, urgent coronary angioplasty was done. After crossing the lesion with workhorse wire, thrombo-suction was done and stented with third generation drug eluting stent. The patient was stable after percutaneous coronary intervention, symptoms subsided and no intra and post procedure complication were noted. The patient was discharged next day. All tests and treatments during hospitalization were performed only after obtaining the patient's informed consent.

Awareness of cardiovascular disease in women has risen over the past decade, yet cardiovascular risk still tends to be underestimated by both the public and health care practitioners, (6) especially among younger women, highlighting the need to develop sex‐specific approaches to optimize treatment of cardiovascular disease in women. Also of concern is the rise in the incidence of acute MI among younger women (< 35 years old) (7). It is likely due to the following multiple risk factors such as smoking, obese, hypertension, diabetes, hyperlipidaemia (higher level of low-density lipoprotein-cholesterol (LDL-C)), higher level of uric acid, history of coronary artery disease, family history of premature AMI, non-obstructive coronary artery disease (CAD), and genetic polymorphisms related to blood coagulation, fibrinogen, homocysteine, being present (8,9). Alongside established cardiovascular risk factors, several other factors appear to contribute to cardiovascular risk among women. These include psychosocial, economic, social, and cultural factors, as well as obstetric and gynaecological history.

In our case we reported a 38 years-old female who suffered from STEMI due to atherosclerotic plaque rupture. This patient suffered from neither hereditary disease, including FH, nor cardiovascular diseases, including previous anginal attack or Kawasaki diseases. In this case, suspected STEMI risk factors include obstetrical history of Dilatation & Curettage procedure. Anaesthesia and surgical trauma can lead to surges in catecholamines, cortisol, and inflammatory cytokines. Perioperative hemodynamic fluctuations can lead to an ischemic imbalance in myocardial oxygen supply and demand that results in myocardial injury. Tachycardia decreases the duration of diastole and increases myocardial wall stress and oxygen requirements. Episodes of hypertension increase left ventricular afterload and increase myocardial oxygen demand. Increases in coronary artery sheer stress may destabilize preexisting coronary atherosclerotic lesions and provoke plaque disruption (erosion or rupture) (10-11).

In a single-centre study of 2018 patients ≥65 years of age or ≥45 years of age with a history of vascular disease, 16% of the patients developed Myocardial injury after non cardiac surgery (MINS) (12). Overall, in a recent systematic review of 169 published studies reporting outcomes of 530867 surgeries, the pooled incidence of MINS was 18% (95% CI, 16%–20%).12 In an analysis restricted to large, prospective series with systematic cTn measurement, 20% (95% CI, 18%–21%) of surgeries were complicated by MINS (12-13).

Preoperative cardiovascular risk assessment may identify patients with an increased likelihood to develop MINS. Estimates of perioperative risk can guide perioperative management and provide data for use during informed consent for surgery and anaesthesia. Patients at increased risk of MINS may warrant modifications in intraoperative care, including invasive arterial pressure monitoring, hypotension avoidance strategies, and systematic preoperative and postoperative cTn surveillance. the incidence of MINS also depends on whether systematic postoperative cTn surveillance is performed because 84% to 93% of patients with MINS have no identifiable ischemic symptoms (14). The type of cTn assay used affects the incidence of MINS, with a higher incidence associated with high-sensitivity cTn compared with conventional assays. In a systemic review of studies that implemented routine postoperative cTn surveillance, the incidence of MINS was 25% with hsTnT assays, 20% with conventional (third- or fourth generation) cTnI assays, and 17% with conventional. TnT assays (12). Finally, the surgical population also affects MINS incidence, which may vary according to age, sex, renal function, and the urgency of surgery (13-14).

This case report highlights the importance of pre operative assessment before any surgery even in low surgical risk patients. However, there are no clear guidelines for pre operative assessment in young patients without any comorbidity, still meticulous examination and risk factor assessment should be done in every patient pre operatively. Efforts to improve recognition and understanding of myocardial injury after non cardiac surgery will ultimately improve postoperative outcomes.

This case highlights the importance of thorough evaluation and management of chest pain in young patients, even in the absence of significant risk factors for cardiovascular disease. It is important to note that the exact cause of STEMI in this patient would require further investigation, including a more detailed clinical evaluation, laboratory tests and imaging studies, to identify any underlying conditions or risk factors. Additional investigation to determine specific mechanisms of MINS is necessary to develop targeted therapies. High-risk individuals having noncardiac surgery should have serial cardiac biomarker assessment during the first 48 to 72 hours postoperatively while hospitalized. At present, it is reasonable to intensify therapy for the secondary prevention of cardiovascular disease in patients with a diagnosis of STEMI post-surgery, particularly for patients with established cardiovascular disease or those who meet existing clinical practice guideline recommendations for therapy. Prompt evaluation, appropriate treatment and close follow-up are crucial in managing these patients.

Consent statement

Written informed consent for the publication of clinical details and clinical images was obtained from the patient.

Data availability

Not applicable.

Declaration of competing interest

The authors declare that there is no conflict of interest.

Acknowledgments

None.

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