Cases reported "Myocardial Infarction"

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1/143. Recurring myocardial infarction in a 35 year old woman.

    A 35 year old woman presented with acute myocardial infarction without any of the usual risk factors: she had never smoked; she had normal blood pressure; she did not have diabetes; plasma concentrations of total cholesterol and high and low density lipoprotein cholesterol, fibrinogen, homocysteine, and Lp(a) lipoprotein were normal. She was not taking oral contraceptives or any other medication. coronary angiography showed occlusion of the left anterior descending coronary artery but no evidence of arteriosclerosis. Medical history disclosed a previous leg vein thrombosis with pulmonary embolism. Coagulation analysis revealed protein c deficiency. The recognition of protein c deficiency as a risk factor for myocardial infarction is important as anticoagulation prevents further thrombotic events, whereas inhibitors of platelet aggregation are ineffective.
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2/143. Primary percutaneous transluminal coronary angioplasty performed for acute myocardial infarction in a patient with idiopathic thrombocytopenic purpura.

    A 72-year-old female with idiopathic thrombocytopenic purpura (ITP) complained of severe chest pain. electrocardiography showed ST-segment depression and negative T wave in I, aVL and V4-6. Following a diagnosis of acute myocardial infarction (AMI), urgent coronary angiography revealed 99% organic stenosis with delayed flow in the proximal segment and 50% in the middle segment of the left anterior descending artery (LAD). Subsequently, percutaneous transluminal coronary angioplasty (PTCA) for the stenosis in the proximal LAD was performed. In the coronary care unit, her blood pressure dropped. Hematomas around the puncture sites were observed and the platelet count was 28,000/mm3. After transfusion, electrocardiography revealed ST-segment elevation in I, aVL and V1-6. Urgent recatheterization disclosed total occlusion in the middle segment of the LAD. Subsequently, PTCA was performed successfully. Then, intravenous immunoglobulin increased the platelet count and the bleeding tendency disappeared. A case of AMI with ITP is rare. The present case suggests that primary PTCA can be a useful therapeutic strategy, but careful attention must be paid to hemostasis and to managing the platelet count.
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3/143. survival without surgical repair of acute rupture of the right ventricular free wall.

    rupture of the myocardial free wall is an infrequent complication of acute myocardial infarction. Unless it occurs in a space confined by pericardial adhesions, only surgical emergency repair of ruptured myocardium can prevent death. In this paper we report the case of an 81-year-old woman who was admitted to the emergency room with cardiac tamponade, resulting from inferolateral acute myocardial infarction and a subsequent rupture of the right ventricular free wall, with the formation of pericardial thrombus and effusion. The patient refused to undergo any surgical or invasive intervention, and therefore she was only treated conservatively. Nevertheless, her condition improved dramatically, as her blood pressure increased and echocardiography abnormalities almost disappeared. Follow-up echocardiography 7 months post discharge was unremarkable. We believe that this rare case emphasizes that in special circumstances, such as creation of a thrombus that prevents more blood from extravasating, free-wall rupture without surgical repair is compatible with long-term survival.
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4/143. Concurrent administration of amrinone with nitric oxide most improves PaO2/FiO2 in acute respiratory and cardiac failure.

    A 55-year-old man developed acute respiratory failure, pulmonary hypertension and left heart failure due to acute myocardial infarction. nitric oxide (NO) inhalation improved arterial oxygenation, decreased pulmonary arterial pressure and increased cardiac output (CO), but combined use of dobutamine with NO produced increases in pulmonary arterial pressure and pulmonary capillary wedge pressure (PCWP). In this patient, amrinone decreased pulmonary arterial pressure and PCWP, and increased PaO2/FiO2 effectively while increasing CO. Combined use of inhaled NO and intravenous amrinone may have beneficial effects for a patient with acute respiratory and cardiac failure.
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5/143. Posterior myocardial infarction complicated by rupture of the posteromedial papillary muscle.

    A 61-year-old man was admitted with acute posterior myocardial infarction and, on physical examination, was shown to have a mitral regurgitation (MR) murmur. Transthoracic echocardiography (TTE) showed severe hypokinesis of the posterior wall and severe MR by color flow. Right heart catheterization with a balloon-tipped catheter revealed a pulmonary artery wedge pressure of 30 mmHg. No 'step-up' was seen in blood samples from the right atrium and right ventricle. On angiography, a subtotal occlusion of the mid circumflex artery was found which was angioplastied and stented. As the patient's clinical condition did not improve, he underwent transesophageal echocardiography (TEE) for further evaluation. This showed complete rupture of the posteromedial papillary muscle. The patient underwent urgent surgery with successful mitral valve replacement. The postoperative course was uncomplicated, and clinical improvement seen. This case report underscores the value of TEE in accurate preoperative diagnosis of papillary muscle rupture by providing preoperative anatomic details of the mitral valve apparatus and surrounding structures.
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6/143. Accelerated transplant coronary artery disease and massive silent acute myocardial infarction in a heart transplant patient--a case report and brief review of literature.

    This case report describes an aggressive form of accelerated atherosclerosis predicted early after transplant by dobutamine stress echocardiography in a patient who died of massive myocardial infarction 32 months after transplantation. The main objective finding of this event was markedly increased cardiac filling pressures during an elective cardiac catheterization and coronary angiography. The literature is briefly reviewed.
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7/143. Idiopathic thrombocytopenic purpura treated with steroid therapy does not prevent acute myocardial infarction: a case report.

    We report the case of a 65-year-old man affected by idiopathic thrombocytopenic purpura, who developed an acute myocardial infarction after 2 years of steroid therapy. thrombocytopenia was initially recognized 11 years earlier, and became severe during the past 2 years [platelets (PLTS) 10000-30000/microl]. He was treated with steroids, initially to perform a surgical procedure (prednisone 75 mg/day), subsequently to maintain a platelet count of about 50000/microl (prednisone 12.5 mg/day). After 1 year of treatment, he began to complain about exertional angina and dyspnea. His blood pressure became elevated and cholesterol level raised. The exercise electrocardiogram, previously manifesting ischaemic changes, normalized after 1 month of steroid wash-out; however, steroid therapy was reinstituted (prednisone 5 mg per day). One year later, he suffered an infero-lateral non-Q-wave myocardial infarction. It seems likely that the severe coronary atherosclerosis present in our patient developed despite a low platelet count, under the spur of a heavier risk factor profile. Steroid therapy could have had a role as a precipitating agent of the acute event, and the opportunity of alternative treatments is considered.
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8/143. Stanford type A acute dissection developing acute myocardial infarction.

    A 75-year-old female, exhibiting epigastric pain and vomiting, underwent treatment for acute gastritis. She also experienced incontinence of urine and chest pain. A diagnosis of acute myocardial infarction was made upon examination of electrocardiographic findings and the patient was transferred to our hospital. Diffuse infarction of the left ventricle and acute aortic dissection (Stanford type A) were diagnosed by electrocardiographic and echo-cardiography. An emergency operation was performed. After induction of anesthesia, elevation of pulmonary artery pressure and fall of pulse pressure were observed, indicating acute cardiac tamponade. Transesophageal ultrasonography disclosed the entry of dissection in the descending aorta. dissection of the aorta extended proximally up to the annulus of the aortic valve and the right and left coronary arteries were compressed by its aneurysm. As aortic insufficiency was mild, only reconstruction of the ascending aorta was carried out. The patient was discharged in fair condition one month after operation under use of postoperative long-term administration of catecholamines.
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9/143. Cold pressure test producing coronary spasm, coronary thrombosis and myocardial infarction in a patient with IgM antibodies against Coxsackie B virus.

    Several lines of evidence have shown that viral infections are capable of causing coronary spasm and precipitating or mimicking clinical myocardial infarction. Here we report the case of a 41-year-old woman with recurrent angina who was admitted to our hospital because of ventricular tachycardia. Laboratory examination revealed positive IgM titers against Coxsackie B virus. coronary angiography showed normal coronary arteries, but following a cold pressure test severe spasm of all coronaries with thrombotic occlusion of the second marginal branch of the circumflex artery occurred. We conclude that coronary spasm should be clinically suspected in patients with chest pain and ventricular arrhythmia in combination with IgM antibodies against Coxsackie B virus. In these patients, a cold pressure test should be avoided, and antithrombotic and antispastic therapy is recommended.
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10/143. Hypertensive crisis and myocardial infarction following massive clonidine overdose.

    OBJECTIVE: To describe a patient who experienced a hypertensive crisis and myocardial infarction following a massive dose of parenteral clonidine. CASE SUMMARY: A 62-year-old white woman with stage 3 breast cancer metastatic to the spine and a history of hypertension received a combined injection of hydromorphone 48.3 mg and clonidine 12.24 mg subcutaneously in an attempt to refill an implanted epidural infusion pump. She promptly developed mental deterioration, blurred vision, worsening respiration, tachycardia, and hypertension. She was immediately treated with naloxone, but subsequently experienced hypertensive urgency, a short-duration tonic-clonic seizure, and an anteroseptal myocardial infarction. cardiac catheterization showed no arteriolar narrowing or blockage, but an anterior infarct was confirmed. DISCUSSION: clonidine is a commonly used alpha-adrenergic agonist. At usual oral doses of 0.2-2 mg/d, it acts centrally to produce hypotensive effects; at doses >7 mg/d, it acts peripherally to stimulate alpha1- and alpha2-adrenergic receptors, leading to vasoconstriction and increased blood pressure. These effects are not easy to control by standard medical therapies and can cause significant morbidity. CONCLUSIONS: clonidine, although a safe medication with usual dosages, must be used with caution when given in injectable form. An overdose of this alpha-adrenoreceptor agonist can produce significant vasospasm and hypertensive emergency. Drugs used to treat overdose, such as naloxone, can potentiate clonidine's adverse effects, leading to further morbidity.
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