Cases reported "Myocardial Infarction"

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1/254. Case study: analysis of an acute anterior-lateral myocardial infarction in a 16-year-old patient with familial hypercholesterolemia.

    This article presents a case study of a 16-year-old male patient with a significant family history for hypercholesterolemia and coronary artery disease, who suffered an anterior lateral myocardial infarction. On admission, his electrocardiograms revealed the classic pattern of an anterior lateral acute myocardial infarction plus a left anterior hemiblock. His cholesterol level was 750 mg/dL, and his low-density lipoprotein was 650 mg/dL. He underwent a cardiac catheterization that revealed an occluded left anterior descending artery requiring a percutaneous transluminal angioplasty and three coronary stents. The 12-lead electrocardiograms on admission and before discharge are analyzed. This article discusses the electrocardiogram characteristics of anterior lateral wall myocardial infarction coupled with a left anterior hemiblock.
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2/254. myocardial infarction-induced ventricular aneurysm in the presence of complete left bundle branch block: a case report suggesting a new electrocardiographic diagnostic criterion.

    A 65-year-old man who had suffered an anterior myocardial infarction (MI) 10 years ago, complicated by a ventricular aneurysm (VA), and subsequently many years later developed complete left bundle branch block (LBBB), is described, with main emphasis on the feasibility of the electrocardiographic (ECG) diagnosis of VA in the presence of this conduction abnormality. Ventricular aneurysm in our patient was repeatedly confirmed by echocardiography over the intervening years. During the time the patient maintained normal intraventricular conduction, the ECG showed persisting ST-segment elevations in the precordial leads. After the development of LBBB, the ECG displayed accentuated ST-segment elevations in the precordial leads with predominantly negative QRS complexes, and ST elevation in V5, despite its primarily positive QRS complex. The authors extend the findings from the previous literature on the diagnosis of acute MI in patients with LBBB or right intraventricular pacing, and the concept of primary and secondary repolarization changes, to the diagnosis of VA in the presence of LBBB.
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3/254. Spontaneous coronary artery dissection. Case report and literature review.

    Primary coronary artery dissection occurring 2 months post partum in a 33-year-old woman is described. Owing to suspected acute myocardial infarction, the patient was treated with thrombolytic therapy but her condition deteriorated. coronary angiography showed dissection of the left anterior descending artery (LAD). Her condition stabilized during treatment with intravenous heparin, aspirin, nitrates, beta-blockers, digoxin, ACE inhibitor and anticoagulants. At discharge she had no symptoms of heart failure. One hundred and forty one cases from the literature are reviewed with special reference to patient characteristics, patient treatment, and prognosis. Primary spontaneous coronary artery dissection is a rare condition but one that must be considered when young people, especially post partum women, present an acute ischaemic syndrome. thrombolytic therapy may be a two-edged sword and therefore early angiography should be considered in making the diagnosis and choosing the therapy.
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4/254. Isolated trigeminal neuropathy due to trigeminal nerve root hemorrhage.

    BACKGROUND: Isolated trigeminal neuropathy is uncommon; causes include trauma, inflammation, or neoplasm. methods: We report a patient who fell and struck his head during a myocardial infarction, was treated with streptokinase, and developed symptoms and signs of an isolated trigeminal sensory neuropathy. RESULTS: Imaging showed hemorrhage in the trigeminal nerve root; follow-up imaging showed resolution of the hemorrhage, but no underlying structural lesion. CONCLUSION: A combination of head trauma plus thrombolysis resulted in an isolated trigeminal neuropathy.
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5/254. Impending acute myocardial infarction during severe exercise associated with a myocardial bridge.

    A young man had an impending acute myocardial infarction while playing soccer. chest pain and anterior ST-segment elevation lasted 3 hours despite anti-ischemic medication, including streptokinase thrombolysis. An electrocardiogram recorded after the symptoms had passed was normal. There was a minimal increase in cardiac enzyme levels, and a pyrophosphate scan and echocardiogram were normal. Coronary cineangiography showed normal coronary arteries except for systolic compression of the left anterior descending coronary artery. An exercise stress test, while the patient was on atenolol, showed absence of myocardial ischemia. This impending acute myocardial infarction could have been caused by an acute thrombus with lysis prior to catheterization or by a deep muscle bridge that kinked or twisted the coronary artery due to myocardial forceful muscular contraction during the sympathetic stimulation of exercise. In conclusion, an impending acute myocardial infarction may occur in young patients having myocardial bridges, and a beta-blocker must be administered, especially when this condition appears during severe exercise.
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6/254. Dynamic left ventricular outflow tract obstruction in acute coronary syndromes: an important cause of new systolic murmur and cardiogenic shock.

    Dynamic left ventricular outflow tract (LVOT) obstruction has traditionally been associated with hypertrophic obstructive cardiomyopathy. Recently, acute dynamic LVOT obstruction has been described as a complication of myocardial infarction (MI). Herein the cases of 3 patients are described, all of whom presented with a systolic murmur and electrocardiographic evidence of MI. All 3 patients developed cardiogenic shock and were subsequently found by echocardiography to manifest an acute dynamic LVOT obstruction. Cardiogenic shock persisted until therapy was directed toward decreasing the degree of the dynamic LVOT obstruction. The treatment of acute coronary syndromes in the presence of a dynamic LVOT obstruction differs from the traditional treatment of acute coronary syndromes and includes the use of beta-blockers and alpha1-agonists, as well as the avoidance of therapies that aggravate the magnitude of the LVOT obstructive gradient, including nitrates, inotropic agents, and afterload reduction. The development of a systolic murmur in the setting of acute MI complicated by cardiogenic shock with only a small elevation in creatine kinase suggests the presence of a dynamic LVOT obstruction, as well as the classical mechanical complications of MI, namely, ventricular septal rupture and papillary muscle rupture. The presence of a dynamic LVOT obstruction is reliably detected by transthoracic echocardiography or by transesophageal echocardiography if transthoracic image quality is suboptimal.
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7/254. Pseudo A-V block. Part II.

    This vignette demonstrates the importance of analyzing arrhythmias in the context of their particular clinical setting. Analysis and treatment of an arrhythmia without clinical information leads to errors in judgment. Arrhythmias may be interpreted as a didactic exercise that is used in the process of teaching and learning. However, when the question is asked, "How do you treat this arrhythmia?", then all clinical information ambient to the arrhythmia in question has to be available for analysis and judgment.
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8/254. Atrial infarction is a unique and often unrecognized clinical entity.

    A patient with heart failure and acute atrial fibrillation received the final diagnosis of atrial infarction associated with ventricular infarction based on clinical findings of ischemia in association with atrial fibrillation and heart failure (mechanisms probably involved: contractile dysfunction and loss of atrial contribution). Although a transesophageal echocardiography, which could refine the diagnosis of anatomic abnormalities, was not performed, all evidence led to the diagnosis of atrial involvement. Electrocardiographic findings were consistent with Liu's major criterion 3. Therapy with digitalis, quinidine and angiotensin-converting enzyme inhibitors was chosen, as the patient had acute pulmonary edema. The use of beta-blockers and verapamil was res-tricted. No other complications, such as thrombo-embolism or atrial rupture, were noted.
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9/254. Beware of the heart: the multiple picture of cardiac involvement in myositis.

    A 42-yr-old woman with dermatomyositis had two myocardial infarctions, episodes of acute chest pain and an acute lung oedema. These events were initially misinterpreted as atherosclerotic ischaemic heart disease accompanying the autoimmune disease. The lack of improvement of cardiac symptoms with anti-ischaemic and immunosuppressive drugs indicated other mechanisms. Intracoronary drug provocation as well as myocardial biopsy revealed a coincidence of small-vessel disease and vasospastic angina as a cause for the severe cardiac symptoms. After initiating therapy with high doses of calcium channel blockers, marked improvement of cardiac symptoms occurred. In the pathogenesis of cardiac involvement in dermatomyositis, two different mechanisms should be considered: inflammatory processes due to dermatomyositis and vasoconstriction caused by an impaired regulation of vascular tone, such as abnormal vessel reactivity or disturbed neuropeptide release. Signs of this generalized vasopathy are Raynaud's phenomenon, Prinzmetal's angina and small-vessel disease, which can coincide. In patients with severe cardiac symptoms and autoimmune diseases, Prinzmetal's angina should be excluded by intracoronary drug provocation using acetylcholine.
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10/254. Systolic anterior movement of mitral valve during acute apical myocardial infarction: An unusual mechanism of acute mitral regurgitation.

    We describe a singular case of a 75-year-old woman affected by an anterior acute myocardial infarction in the subset of a very recent orthopaedic surgery. She had had severe mitral regurgitation on coronary angiography. A thorough cardiac echocardiographic examination revealed the particular mechanism of mitral incompetence, consisting of a dynamic anterior mitral leaflet displacement caused by a sustained compensatory left ventricle hypercontractility and favored by postsurgical moderate anemia and mild hypertensive hypertrophy. The use of beta-blockers and the avoidance of pure vasodilators permitted complete reversal of such mechanisms during the clinical course.
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