European Journal of Cardiovascular Medicine

Chest pain is one of the most frequent and potentially life-threatening complaints presenting in emergency departments worldwide. It encompasses a broad differential diagnosis, ranging from benign musculoskeletal causes to critical cardiovascular emergencies such as acute coronary syndrome (ACS), pulmonary embolism, or aortic dissection [1,2]. Rapid assessment and accurate diagnosis are vital to ensure timely intervention and prevent mortality [3]. This case report discusses a 56-year-old Hindu male who presented with sudden onset chest pain, highlighting the diagnostic approach, differential considerations, and clinical management. Through this case, we aim to emphasize the importance of early recognition of alarming features, judicious use of diagnostic tools, and evidence-based decision-making in acute chest pain scenarios [4]. Such reports not only contribute to clinical knowledge but also offer insights into varied presentations that can aid in improving patient outcomes in similar real-world settings [5].

A 56-year-old Hindu male presented with complaints of chest pain for the past 2 days and shortness of breath for 1 day. The chest pain was sudden in onset while he was engaged in routine activities. It was retrosternal in location, diffuse, constricting, and heavy in nature, radiating to the jaw and left arm. The pain was persistent and unrelieved by rest, positional changes, or leaning forward. Associated symptoms included nausea, profuse sweating, and a sense of inner restlessness. There was no history of cough, sputum production, trauma, syncope, neurological deficits, or symptoms related to food intake or posture. Shortness of breath (NYHA Class II) developed a day later, was exertional, and improved with rest. There were occasional palpitations but no orthopnea, paroxysmal nocturnal dyspnea, wheeze, fever, or peripheral edema. His condition progressively worsened, leading to admission at the district hospital and subsequent referral to AGMC and GBP Hospital.

History of Present Illness

The patient experienced a sudden onset of chest pain while performing routine duties, which persisted for two days. The pain was retrosternal, diffuse, heavy, and constricting, with radiation to the jaw and left upper limb. It was unrelieved by rest, positional changes, or forward bending. The episode was accompanied by nausea, diaphoresis, and a feeling of restlessness. There were no symptoms of cough, sputum, syncope, focal neurological deficits, food-induced reflux, or trauma. No variation was noted with posture or time of day. Over the following day, the patient developed shortness of breath (NYHA Class II), which worsened with activity and improved with rest. He also reported occasional palpitations. The dyspnea was not associated with orthopnea, paroxysmal nocturnal dyspnea, cough, wheezing, fever, or edema. As symptoms worsened, he sought medical attention at a district hospital before being referred for further management.

History of Past Illness

The patient denied any previous similar episodes. He had no history of ischemic heart disease, heart failure, valvular disease, diabetes mellitus, hypertension, thyroid disorders, or tuberculosis. No significant past medical or surgical history was noted.

DIAGNOSIS AND MANAGEMENT

The patient was initially managed as a case of acute coronary syndrome with features suggestive of an acute inferior wall myocardial infarction. Emergency treatment included oxygen inhalation support and administration of low molecular weight heparin (60 mg subcutaneously twice daily) to prevent thrombus propagation. Dual antiplatelet therapy (DAPT) with a loading dose of aspirin and clopidogrel was initiated, followed by maintenance therapy. High-intensity statin therapy with atorvastatin 80 mg was administered stat and continued once daily at night. A beta-blocker, bisoprolol 2.5 mg once daily, was added to reduce myocardial oxygen demand. Gastroprotection was ensured with pantoprazole 40 mg once daily on an empty stomach. Mineralocorticoid receptor antagonist (MRA) eplerenone 25 mg once daily was also initiated. Supportive measures included soft diet, stool softeners, and lifestyle modification advice. The patient showed symptomatic improvement with this regimen. Following stabilization, further evaluation was carried out which led to the diagnosis of Polycythemia Vera. Consequently, cytoreductive therapy with hydroxyurea 500 mg twice daily was started. In addition, the patient underwent two sessions of therapeutic phlebotomy during hospitalization, with instructions to maintain adequate hydration—specifically, one liter of fluid intake before and after each session. Smoking cessation was strongly advised to reduce cardiovascular risk. The patient responded well to the combined management of myocardial infarction and Polycythemia Vera, and was planned for coronary angiography. He was discharged in stable condition with instructions for regular follow-up and continued medical supervision.

Respiratory System Examination

On examination of the respiratory system, the upper respiratory tract appeared normal with no abnormalities noted. Inspection of the lower respiratory tract revealed a bilaterally symmetrical and elliptical chest contour. The overlying skin was normal with no visible scars, pulsations, venous engorgement, or chest wall indrawing. Chest movements were equal and synchronous on both sides during respiration. On palpation, the trachea was found to be centrally positioned, and there was no tenderness over the chest wall or costochondral junctions. Vocal fremitus was equal bilaterally, indicating uniform transmission of vocal vibrations. Chest expansion was measured to be 3 cm, which is within normal limits. Percussion elicited a resonant note over all lung fields bilaterally, suggesting normal underlying lung parenchyma. Auscultation revealed normal vesicular breath sounds in both lung fields, with the presence of fine crepitations in the basilar region of the left lung, possibly indicating localized fluid or early consolidation. Vocal resonance was normal across all lung zones bilaterally.

FINAL DIAGNOSIS

ACUTE INFERIOR WALL MYOCARDIAL INFARCTION SECONDARY TO POLYCYTHEMIA VERA

After thorough clinical evaluation, supportive electrocardiographic changes, and elevated cardiac biomarkers, the patient was diagnosed with Acute Inferior Wall Myocardial Infarction (IWMI). Further hematological investigations revealed elevated hemoglobin and hematocrit levels, along with the presence of JAK2 V617F mutation, confirming a diagnosis of Polycythemia Vera—a myeloproliferative neoplasm characterized by increased red cell mass and hyperviscosity. The hypercoagulable state induced by Polycythemia Vera was identified as the underlying predisposing factor for coronary thrombosis, leading to the acute myocardial infarction. Therefore, the final diagnosis was made as Acute Inferior Wall Myocardial Infarction secondary to Polycythemia Vera.

Polycythemia Vera (PV) is a chronic myeloproliferative neoplasm characterized by clonal proliferation of hematopoietic stem cells, leading to increased production of red blood cells, granulocytes, and platelets in the absence of a physiological stimulus [1]. The pathogenesis of PV is largely attributed to the JAK2 V617F mutation, a gain-of-function mutation in the pseudokinase domain of the JAK2 tyrosine kinase gene, resulting in constitutive activation of the JAK-STAT signaling pathway [2]. Less commonly, mutations in exon 12 of JAK2, CALR, LNK, or other molecular markers may be identified [3]. According to the 2016 WHO diagnostic criteria, PV is diagnosed when all three major criteria are met or two major plus one minor criterion [4]. The major criteria include hemoglobin >16.5 g/dL in men or >16 g/dL in women (or hematocrit >49% in men, >48% in women), bone marrow biopsy showing panmyelosis, and the presence of a JAK2 mutation. The minor criterion includes subnormal serum erythropoietin levels. PV may be discovered incidentally or may present with symptoms due to hyperviscosity, including vertigo, tinnitus, visual disturbances, headache, or transient ischemic attacks [5]. Vascular complications such as erythromelalgia, digital ischemia, and both venous and arterial thromboses are known manifestations of the disease [6]. Cardiovascular events like myocardial infarction, although relatively rare, are serious complications [7]. In PV, hyperviscosity and endothelial dysfunction lead to increased thrombotic risk, and coronary thrombosis can precipitate acute coronary syndromes including myocardial infarction, as seen in this patient. Management includes therapeutic phlebotomy to reduce hematocrit, and cytoreductive therapy with agents such as hydroxyurea, interferon-alpha (preferred in patients under 40 years), or ruxolitinib in high-risk patients [8]. In cases of myocardial infarction associated with PV, standard interventional strategies like stenting may need to be carefully considered due to the elevated risk of stent thrombosis related to increased blood viscosity and platelet activation.

The clinical presentation was highly suggestive of a cardiac origin of chest pain, necessitating urgent evaluation and management. This case highlights the importance of comprehensive symptom analysis and prompt referral in patients with atypical chest pain, especially in the absence of prior comorbidities.

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