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 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a case of arterial coronary embolism by calcified material of a bioprosthesis of bovine pericardium of the INC in aortic position 8 years after its implantation. Echocardiogram and catheterization with coronarography demonstrated prosthetic aortic dysfunction and normal coronaries. The patient complained of stable angor and dyspnea. During coronarography there was an increase of symptoms together with ECG changes and after a few hours with enzymatic increase. The patient was brought urgently to surgery where mitroaortic prosthesis was changed with mechanic prosthesis. As surgical findings: absence of a leaflet of prosthesis in aortic position with free fragmented calcium in periannular region and two remaining leaflet completely calcified, prosthesis in mitral position of normal appearance. We conclude that ischemia or myocardial infarction in presence of normal coronaries in patients with bovine pericardial bioprosthesis in aortic position can be secondary to calcium embolism, originated by mineralization process of a degenerated bioprosthesis several years after its implantation.
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PMID:[Calcified embolism of the coronary artery due to the degeneration of a bioprosthesis in the aortic position]. 829 26

The concepts of chronobiology and chronopharmacology have become more and more important in medical practice nowadays. Today, the circadian variation in blood pressure and heart rate as well as in the occurrence of acute cardiovascular disease is quite obvious (ischemia, infarction, stroke and sudden death). However, biological rhythms are also present in episodes of dyspnoea in nocturnal asthma, in hormonal pulses, in the organization of the immunological system and in the processes of cellular proliferation. These acknowledgments have been leading to changes in our therapeutical approaches implying the definition of correct anti-hypertensive and anti-ischemic strategy was well as in the use of xanthins, corticosteroids, immunomodulators and cytostatics.
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PMID:[Biological rhythms in man. Particular aspects in medicine]. 848 69

Many patients undergoing investigation for coronary artery disease are unable to exercise adequately due to physical or psychological reasons. Thallium-201 imaging using dipyridamole or adenosine may then be a suitable method of assessing myocardial perfusion. In patients with asthma, these drugs are contraindicated because of the risk of provoking bronchospasm. This study assesses the safety of dobutamine for thallium-201 myocardial perfusion imaging in patients with asthma who were unable to perform adequate exercise. Dobutamine was infused at rates < or = 40 micrograms/kg/min in 30 asthmatic patients for thallium-201 emission tomography. The severity of the airway reactivity ranged from mild to severe (bronchodilator treatment ranging from inhaled beta 2 agonists alone to maximal therapy including oral steroids). Coronary angiography was performed in 20 patients. Minor side effects of dobutamine were frequent, but did not limit the infusion rate. There were no episodes of bronchospasm, but tolerable dyspnea occurred in 8 patients who had reversible ischemia; this rapidly resolved with termination of the infusion. There were no serious cardiac complications, but chest pain occurred in 67% of patients. Thallium-201 images were abnormal in 10 of 11 patients with coronary artery disease (sensitivity 91%) and normal in 7 of 9 with normal coronary arteries (specificity 79%). Dobutamine thallium-201 myocardial perfusion tomography is a safe procedure in patients with asthma.
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PMID:Safety of dobutamine stress for thallium-201 myocardial perfusion tomography in patients with asthma. 849 79

The authors describe a rare case of pulmonary thromboembolism with unusual clinical findings and emphasized the large difficulty encountered in formuling a correct diagnosis in a reasonable time. A man, 60 years old, was admitted to a Medical Division of our hospital for the appearance of chest pain and epigastric pain during effort in the last year. He smoked 20 cigarettes a day and drank wine (1 or 2 litres a day). He was affected by hypercholesterolemia and in the past reported relapsed thrombophlebitis in the left leg. Four years before admission to our hospital he underwent large and small left saphenectomy. He had no cardiac events in the past. After a non significant exercise stress test the patient was treated with nitrates and asa and was discharged from the hospital. At home the symptoms increased and after 8 months the patient was admitted again to the Cardiologic Division of the hospital. At admission he reported dyspnea and chest pain at rest, not only during effort and the ECG showed negative T waves in anterior and inferior leads. Intravenous heparine, nitrates and calcium antagonists stabilized the clinical picture. The following examinations revealed: reduction of the T wave negativity at the ECG registered during chest pain; mild enlargement of the heart at the chest roentgenogram; normal value of the left ventricle and apical and midseptal by ipokinesia at the transthoracic echocardiogram; normal coronary artery at the coronary arteriography. "Vasospastic angina" was diagnosed and the patient was discharged after 20 days, asymptomatic. After 15 days he returned to the hospital again for chest pain, dyspnea, hypotension and syncope despite therapy. At physical examination he showed a painful left tibio-tarsal tumefaction, an increased and splitting second heart sound in the pulmonary area and a systolic murmur in the third and fourth left interspace. The ECG showed a severe anterior ischemia, while a new transthoracic echocardiogram revealed a considerable dilatation of the right atrium, right ventricle and the main pulmonary artery with severe tricuspid regurgitation and pulmonary hypertension (mean PAP about 50 mmHg). The following pulmonary perfusion scintigraphy confirmed the diagnosis of pulmonary embolism and the selective right and left pulmonary arteriography exhibited multiple thrombi and large intravascular filling defects. The right heart catheterization confirmed a chronic precapillary pulmonary hypertension (mean PAP = 55 mmHg). About 24 hours after these examinations the patient died because of a cardiac arrest with electromechanical dissociation. Pulmonary thromboembolism is a potentially fatal disease characterized by a largely variable clinical presentation. Frequently pulmonary embolism diagnosis is difficult especially when clinical findings are unusual. In the case observed the "typical" chest and epigastric pains associated with the electrocardiographic findings directed diagnosis towards myocardial ischemia. Also after the coronary arteriography that showed normal coronary artery, the erroneous diagnosis persisted. Pulmonary embolism was correctly diagnosed too late to begin an effective therapy. These unusual clinical findings and diagnostic mistakes are stressed and critically reviewed in the article.
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PMID:[Pulmonary thromboembolism. A clinical case with unusual presentation]. 871 Jan 39

The dissection is termed Type A according to the Stanford classification, if the ascending aorta is involved. It is termed type B, if the ascending aorta is not involved. Most patients with Type A aortic dissection die from intrapericardial rupture with cardiac tamponade, free pleural rupture, massive aortic regurgitation, or coronary or cerebral malperfusion (ischemic heart disease or stroke). Most patients with Type B dissection die from free pleural rupture or renal or visceral vascular complications. The resultant compromise of various aortic branches (inomunate, carotid, subclavian, spinal, renal, superior mesentric, or iliac arteries) results in a wide variety of symptoms and signs (shock, dyspnea, stroke, paraplegia, anuria, abdominal pain or extremity ischemia).
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PMID:[Pathophysiology and complications of aortic dissection]. 896 89

Three complications which influence both survival and quality of life in transplanted patients will be the object of this chapter. Graft dysfunction: this is a severe re-implantation oedema leading to inefficiency of the graft as regards haemostasis whether or not associated with haemodynamic complications. The liberation of free radicals and/or cytokines induced by ischemia-reperfusion of the graft plays an important role in the pathogenesis of this syndrome. Acute rejection: the mechanism is complex leading to the intervention of an immune response stimulated by the detection of allo-antigens. The clinical picture is often non-specific. Treatment requires boluses of methyl prednisolone completed by decreasing dose of corticosteroid therapy orally. The syndrome of bronchiolitis obliterans: this is a progressive failure of the airways. This syndrome occurs in the long term in 50% of patients and presents with progressive dyspnoea associated with persistent or recurrent cough. The pathogenesis is brought about principally by a chronic rejection with a specific cytotoxic reaction of T lymphocytes against the airway epithelium which expresses Class II major histocompatibility antigens. Attempts at curative treatment can be extremely deceptive and leads to, at best, a slowing in decline of respiratory function.
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PMID:[Graft dysfunction, acute rejection and bronchiolitis obliterans in lung and heart-lung transplantation]. 901 9

Arbutamine is a new catecholamine designed for use as a pharmacologic stress agent. This study compared the sensitivity of arbutamine with symptom-limited exercise to induce echocardiographic signs of ischemia. Arbutamine was administered by a computerized closed-loop delivery system that controls the infusion rate of arbutamine toward a predefined rate of heart rate increase and maximum heart rate limit. Beta blockers were stopped > or = 48 hours before both tests. Stress was stopped for intolerable symptoms, or clinical, electrocardiographic or echocardiographic signs of ischemia (new or worsening wall motion abnormality), target heart rate (> or = 85% age predicted maximum heart rate), or plateau of heart rate response. Thirty-seven patients were entered into the study (35 arbutamine and exercise, 1 arbutamine only, 1 exercise only), of which 30 had angiographic evidence of coronary artery disease (> or = 50% lumen diameter narrowing). Rate-pressure product increased significantly in response to both stress modalities (p < 0.001) and was significantly greater with exercise (11,308 +/- 2,443) than with arbutamine (9,486 +/- 2,479, p < 0.001). The time to maximum heart rate was longer during arbutamine stress echocardiography than during exercise testing (17.3 +/- 9.4 versus 9.3 +/- 4.2 minutes, respectively, p < 0.001). There were more patients with interpretable echo data for arbutamine (82%) than for exercise (67%). Sensitivity for recognition of myocardial ischemia was 94% (95% confidence interval 70% to 100%) and 88% (95% confidence interval 62% to 98%), respectively. The most frequent adverse events during arbutamine (n = 36) were dyspnea (5.6%) and tremor (5.6%). Two arbutamine stress tests were discontinued due to arrhythmias: 1 patient had premature atrial and ventricular beats, and the other had premature atrial contractions and atrial fibrillation. Arrhythmias were well tolerated and resolved without sequelae. In conclusion, the sensitivity of arbutamine to induce echocardiographic signs of ischemia was similar to that of exercise despite a lower rate-pressure product. Arbutamine was well tolerated and provides a reliable alternative to exercise echocardiography.
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PMID:Comparison of arbutamine and exercise echocardiography in diagnosing myocardial ischemia. 907 May 46

The effects of altitude on coronary patients with impaired left ventricular function are virtually unknown and the question arises whether an exposure to altitude poses a risk to such patients. Twenty-three patients with coronary artery disease (mean age 51 +/- 9 years; group H) with a mean ejection fraction of 39 +/- 6% were compared with 23 normal subjects (mean age 53 +/- 6 years; group N). Both groups underwent a maximal symptom-limited bicycle stress test at 1,000 m and 2 days later at 2,500 m. In both groups, exercise capacity decreased significantly (group H, 1,000 m 162 +/- 28 W, 2,500 m 155 +/- 28 W, p = 0.02; group N, 1,000 m 205 +/- 28 W, 2,500 m 198 +/- 25 W, p = 0.02). Maximal heart rate and blood pressure did not differ between 1,000 and 2,500 m; oxygen saturation at rest and during exercise remained unchanged. At 2,500 m, the test was terminated more often because of dyspnea, but the level of perceived exertion (Borg) was similar to that at 1,000 m. There were no complications or signs of ischemia. Thus, patients with coronary artery disease with impaired left ventricular function without residual ischemia have good tolerance to exposure to altitude. The effects in patients are comparable to those in a group of normal subjects and the risk for an adverse event is not increased.
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PMID:Effects of exposure to altitude on men with coronary artery disease and impaired left ventricular function. 946 65

These findings underscore the importance of understanding the complex interactions of multiple-organ systems in a chronic systemic disease state like congestive heart failure. The exaggerated ventilatory response in patients with heart failure is clearly multifactorial and it remains difficult to decipher whether this response results from or contributes to the sensation of dyspnea. Pulmonary dysfunction including ventilation-perfusion mismatching, decreased lung compliance, restriction, airway obstruction, decreased diffusion capacity, and decreases in respiratory muscle strength and endurance contribute to an inefficient breathing pattern and increased work of breathing. This is further compounded by the limited ability of the failing heart to meet the metabolic demands of the respiratory muscles, leading to under-perfusion and ischemia. This imbalance contributes to perceived dyspnea and exercise limitations. Understanding these physiologic cardiopulmonary interactions may lead to therapeutic modalities, such as respiratory muscle training, aimed at disrupting this intertwined cycle of events and improving functional capacity in patients with heart failure.
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PMID:Pulmonary manifestations of chronic heart failure. 955 45

A 69-year-old woman was admitted because of increase of chest pain and dyspnea. Systolic murmur of Levine III/VI was heard. Electrocardiography showed ST depression caused by ischemia. Echocardiography revealed severe mitral regurgitation (MR) and inferoposterior hypokinetic wall motion. Left ventriculography revealed the presence of MR (II/IV). Coronary angiography showed severe organic stenosis of the right coronary artery. Based on these findings, the diagnosis was severe papillary muscle dysfunction caused by unstable angina. The lesion of the right coronary artery was successfully stented with a Palmaz-Schatz stent. During balloon inflation, the v wave of the pulmonary capillary pressure curve was greatly elevated. After the stent implantation, ST depression was normalized and MR improved dramatically. Therefore, we suppose that acute MR was induced by temporary papillary muscle dysfunction, and could be relieved with coronary angioplasty.
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PMID:Marked attenuation of mitral regurgitation by stent implantation: a patient with unstable angina. 966 3


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