ACUTE MYOCARDIAL INFARCTION DUE TO CORONARY THROMBOSIS AS PRESENTATION OF NEOPLASIA
Doenças cardiovasculares - Caso Clínico
Congresso ID: CC015 - Resumo ID: 68
Hospital Pedro Hispano
Ana Catarina Trigo, Marta Vilaça, Liliana Carneiro, Cristina Oliveira, Ana Sofia Correia
INTRODUCTION: Acute myocardial infarction (AMI) is usually related to obstructive coronary atherosclerosis, but spontaneous coronary thrombosis or coronary emboli (CE) can also occur. Pro coagulant states, valvular disease, atrial fibrillation, atrial septal defect with paradoxal embolism, intracardiac tumors, among others, can lead to coronary thrombosis. The prevalence of CE as mechanism of AMI ranges from 4% to 13% according to angiographic or autopsy studies.
CLINICAL CASE: A 77-year-old woman, with background of arterial hypertension and a Bentall surgery eight years before (biologic aortic valve and aortic conduct implantation), presented at emergency department with typical angina at rest. The electrocardiogram showed: sinusal rhythm, ST elevation in leads V2 to V6 and pathologic Q-waves in leads V3 to V5. High sensibility troponin level was 4493.2 ng/L (reference value <15.6 mg/L). No abnormalities were found on the echocardiogram, including the biologic valve and aortic conduct. Angiography revealed a total occlusion at the middle segment of the left descending anterior coronary artery with suspicion of intraluminal thrombus. An eluting-stent was implanted. Both dual antiplatelet therapy and hypocoagulation were initiated, but a normocytic/normochromic anaemia was diagnosed. Further studies revealed: normal coagulation parameters, normal platelet count, iron deficiency and an inflammatory state with a high sedimentation rate (ESR) of 119 mm/1h. No immune disorders were noticed. Digestive endoscopy and colonoscopy were normal. The complete imaging study showed a suspicious nodule on right breast, and its biopsy revealed an infiltrating ductal carcinoma. No findings of metastasis were detected. A serum monoclonal IgG/Kappa protein was identified on electrophoresis, and the plasma viscosity was elevated: 2.13 centipoise (cps) - reference value: 1.5-1.72 cps. Unfortunately the patient died before we could conclude the diagnostic studies.
DISCUSSION: The causal interrelationship between cancer and hypercoagulability state is known since the 19th century, but the underlying mechanisms are still poorly understood. Thrombosis could occur at the moment of neoplasia diagnostic, or even months or years before. The most well recognized presentation of hypercoagulability is deep venous thrombosis and pulmonary embolus, but it may also affect arterial beds. Our patient had no vascular risk factors, no personal nor familial history of thrombotic events, so we focused on acquired pro coagulant states. The high ESR and anaemia made us suspect of a neoplasia, and actually we found a breast cancer and a possible monoclonal gammopathy. We believe our patient’s AMI was due to a hypercoagulability state caused by those both. Some data showed an increased rate of myocardial infarction in people with breast cancer, suggesting that there could be a relationship between both. Data concerning paraproteinemias are more sparse.
CLINICAL CASE: A 77-year-old woman, with background of arterial hypertension and a Bentall surgery eight years before (biologic aortic valve and aortic conduct implantation), presented at emergency department with typical angina at rest. The electrocardiogram showed: sinusal rhythm, ST elevation in leads V2 to V6 and pathologic Q-waves in leads V3 to V5. High sensibility troponin level was 4493.2 ng/L (reference value <15.6 mg/L). No abnormalities were found on the echocardiogram, including the biologic valve and aortic conduct. Angiography revealed a total occlusion at the middle segment of the left descending anterior coronary artery with suspicion of intraluminal thrombus. An eluting-stent was implanted. Both dual antiplatelet therapy and hypocoagulation were initiated, but a normocytic/normochromic anaemia was diagnosed. Further studies revealed: normal coagulation parameters, normal platelet count, iron deficiency and an inflammatory state with a high sedimentation rate (ESR) of 119 mm/1h. No immune disorders were noticed. Digestive endoscopy and colonoscopy were normal. The complete imaging study showed a suspicious nodule on right breast, and its biopsy revealed an infiltrating ductal carcinoma. No findings of metastasis were detected. A serum monoclonal IgG/Kappa protein was identified on electrophoresis, and the plasma viscosity was elevated: 2.13 centipoise (cps) - reference value: 1.5-1.72 cps. Unfortunately the patient died before we could conclude the diagnostic studies.
DISCUSSION: The causal interrelationship between cancer and hypercoagulability state is known since the 19th century, but the underlying mechanisms are still poorly understood. Thrombosis could occur at the moment of neoplasia diagnostic, or even months or years before. The most well recognized presentation of hypercoagulability is deep venous thrombosis and pulmonary embolus, but it may also affect arterial beds. Our patient had no vascular risk factors, no personal nor familial history of thrombotic events, so we focused on acquired pro coagulant states. The high ESR and anaemia made us suspect of a neoplasia, and actually we found a breast cancer and a possible monoclonal gammopathy. We believe our patient’s AMI was due to a hypercoagulability state caused by those both. Some data showed an increased rate of myocardial infarction in people with breast cancer, suggesting that there could be a relationship between both. Data concerning paraproteinemias are more sparse.