Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low gradient aortic stenosis can be caused by critical aortic stenosis causing left ventricular impairment or by more moderate aortic stenosis coexisting with another cause of left ventricular impairment. The main challenges are to differentiate these two states and then to determine whether the left ventricle is likely to recover after aortic valve surgery. Exhaustive echocardiography is necessary, including the use of dobutamine stress. Guideline criteria for severe aortic stenosis are given in this article. The most secure criteria are mean transaortic pressure difference greater than 30 mm Hg and effective orifice area less than 1.2 cm(2) during dobutamine stress. However, the presence of left ventricular contractile reserve more closely determines outcome after surgery than do markers of stenosis. Surgery is most clearly indicated if there is severe aortic stenosis and an increase in the systolic velocity integral by greater than 20% during dobutamine infusion. Preoperative catheterization is necessary to determine coronary anatomy, but the aortic valve should not be crossed because of the relatively high risk of death, stroke, pulmonary edema, and cardiogenic shock. In patients judged too ill for immediate surgery, a period of medical resuscitation with diuretics and dobutamine should be considered. Balloon valvotomy is not indicated.
Curr Treat Options Cardiovasc Med 2003 Dec
PMID:Low Gradient, Low Ejection Fraction Aortic Stenosis. 1457 24

A 51-year-old male with acute fulminating pulmonary edema and cardiogenic shock secondary to severe mitral insufficiency from dislodgment of the disc occluder in a Wada-Cutter valve was treated by immediate open heart procedure with a Bjork-Shiley mitral valve replacement. The patient survived and remains well. This is the second patient reported to survive operation and replacement of a malfunctioning prosthetic mitral valve from which the poppet escaped and embolized. The first case was reported by Hughes et al(1) in February, 1975. Some striking similarities, as well as differences, in these two cases are discussed.
Cardiovasc Dis 1975
PMID:A SECOND CASE OF LATE EMBOLIZATION OF PROSTHETIC MITRAL VALVE OCCLUDER WITH SURVIVAL FOLLOWING REOPERATION. 1521 20

A patient with a dissecting aortic aneurysm, Type 1, developed acute pulmonary edema unexplained by the usual etiologic factors. Pathologic evidence that bronchial arterial circulation was interrupted led us to hypothesize that pulmonary edema could be due to ischemia of the bronchial circulation. To test this hypothesis, two chronic studies were done in dogs. The first study consisted of selective ligation of the right posterior bronchial artery at its origin at the fifth or sixth intercostal artery. After recovery from surgery, biopsies were taken from the ipsilateral and contralateral lung at time periods from 5 hours to 11 days. Ischemic damage was found in seven of eight dogs (87.5%), and was confined to the right lung. Histological examination revealed initial congestion within 8 hours, followed by pulmonary edema within 72 hours, and finally, disruption of alveolar septa with small emphysematous bullae on the eleventh postoperative day. The left lung remained normal in histological appearance. The second study consisted of transplanting the bronchial artery to the pulmonary artery to create a low pressure system and low O(2) content, and to simulate a regional shock situation. In five of six dogs (83.3%), the anastomosis was occluded within 72 hours, probably due to pressure competition from small collateral bronchial circulation. However, in these five dogs, pulmonary vascular resistance increased by 53%, intrapulmonary shunting increased by 83%, and the alveolar-to-arterial oxygen gradient increased by 150 mm Hg. Pulmonary edema was again confined to the right lung. Bronchial arteriograms demonstrated the extensive and variable distribution of the bronchial circulation in dogs. In the sixth dog, the anastomosis remained patent with a left-to-right shunt, due to a larger bronchial arterial collateral circulation. In this animal, the pulmonary arterial resistance, intrapulmonary shunting, and alveolar-arterial O(2) gradient were normal. Pulmonary edema was absent in lung biopsies. Bronchial circulation is discussed with respect to its clinical implications for lung transplants, shock, thoracic aneurysms, and mediastinal surgery. The results of this study suggest that the systemic bronchial circulation is important for normal lung function.
Cardiovasc Dis 1981 Dec
PMID:The ischemic lung: Role of the bronchial arteries in lung function. 1521 75

Although previous reports have attributed acute renal failure (ARF) following cardiovascular surgery to acute tubular necrosis (ATN), little emphasis has been placed on renal failure due to congestive heart failure (CARF). Of 100 cases of ARF studied prospectively over an 18-month period, 36 occurred after open-heart surgery. Nineteen of these cases were associated with heart failure. The remaining 17 had ATN as manifested by high urinary sodium, low urine/plasma creatinine, and abnormal urinary sediment. At the onset of CARF, intravascular volume expansion was universally present, and oliguria with pulmonary edema was common. Urinary chemistries were (mean +/- SD): sodium (mEq/L) 8 +/- 7, U/P creatinine 72 +/- 45, and FENa (%) 0.1 +/- 0.1. Therapy consisted of digoxin, furosemide (F), vasopressors (V), and, when indicated, intraaortic balloon counterpulsation. Survivors of CARF responded more frequently to F and required less V. Ultimately, survival depended upon improvement in cardiac performance. All oliguric ATN patients failed to respond to F. Mortality for the CARF group was 52%. In contrast, 82% of the oliguric ATN group expired, whereas overall ATN mortality was 60%. Cardiogenic acute renal failure is a frequent cause of ARF after open-heart surgery in our institution. It is characterized by prerenal urinary chemistries, has a high mortality, and may be reversible.
Cardiovasc Dis 1979 Sep
PMID:CARDIOGENIC ACUTE RENAL FAILURE (CARF) FOLLOWING OPEN-HEART SURGERY. 1521 6

A 35-year-old man presented to our institution one day after the onset of dyspnea. Coronary angiography revealed the occlusion of the left main trunk. The left main coronary artery and the left circumflex artery were recanalized, but he was hypotensive with low cardiac output. Even after he was placed on circulatory support with veno-arterial extracorporeal membrane oxygenation (ECMO), hemodynamic deterioration could not be reversed, and lung edema developed. The decision was made to use Toyobo LVAS. With institution of left ventricular assist system (LVAS), however, the patient's arterial saturation decreased. Peripheral veno-venous (V-V) ECMO was promptly established, and the patient's arterial saturation improved. On postoperative day 3, the patient was successfully weaned from V-V ECMO. He was extubated on postoperative day 28. The patient was recovered without any serious complications. Although echocardiography showed no substantial improvement in left ventricular function, his general condition is doing quite well with the assist of Toyobo LVAS. He is on rehabilitation program and awaiting heart transplantation.
Jpn J Thorac Cardiovasc Surg 2004 Aug
PMID:Use of an extracorporeal left ventricular assist system after acute myocardial infarction due to occlusion of the left main coronary artery. 1538 16

HIV infection is a global public health issue that is frequently associated with cardiovascular involvement. These HIV-associated cardiovascular manifestations are often clinically occult or attributed incorrectly to other non-cardiac disease processes. A heightened awareness and routine screening for cardiovascular involvement in HIV-infected patients leads to earlier detection and the hope for a reduction in associated morbidity and mortality. Left ventricular dysfunction, an independent predictor of mortality in HIV-infected patients, is the result of many causes in this population and may result in dilated cardiomyopathy and congestive heart failure in about 10% of patients. Other HIV-associated cardiovascular problems include infective endocarditis, cardiovascular malignancy, pulmonary arterial hypertension, vasculitis, pericardial effusion, premature atherosclerosis, and arrhythmias. HIV-associated cardiovascular emergencies include congestive heart failure, pulmonary edema, supraventricular and ventricular arrhythmias, endocarditis, and tamponade. Anti-infective and immunomodulatory therapies may be particularly helpful in this population to reduce associated cardiovascular disease. Highly active antiretroviral therapy may result in lipodystrophy, hyperlipidemia, truncal adiposity, and insulin resistance that can be improved by physical activity and training programs. Cardiovascular complications of therapeutic drugs in HIV-infected patients include torsade de pointes, congestive heart failure, dyslipidemia, accelerated atherosclerosis, and myocardial infarction. In summary, cardiovascular complications are important contributors to morbidity and mortality in HIV-infected patients that can be detected early in many cases and treated effectively.
Am J Cardiovasc Drugs 2004
PMID:HIV-related cardiovascular disease and drug interactions. 1544 73

Most cardiac tumors are benign, whereas up to 50 % of the diagnosed cases are histologically myxomas. The common clinical signs are rhythm disturbances, myocardial ischemia, pulmonary edema, syncope and cardiac arrest. They do normally lead to the diagnostic hypothesis of an intracardiac mass. The primary modality for imaging is echocardiography which usually confirms the suspected diagnosis. But in rare cases there are masses which cannot be exactly identified by this technique. Here we present a patient with an atypical echocardiography of an unusual intracardiac tumor.
Thorac Cardiovasc Surg 2004 Oct
PMID:Cystic tumor in the left atrium: an unusual aspect of a myxoma. 1547 Jun 13

Renal artery stenosis (RAS) is a common condition associated with hypertension and renal insufficiency. The high prevalence of RAS patients with coronary and lower extremity vascular disease has been well established. Fibromuscular dysplasia in young females and atherosclerosis in patients over the age of 55 are the most common causes. Poorly controlled hypertension refractory to medical therapy, worsening of renal function, and flash pulmonary edema may point to underlying RAS. Duplex ultrasonography and magnetic resonance angiography have largely replaced captopril scanning for RAS screening. However, renal angiography still remains the gold standard to diagnose RAS. Treatment options include medical therapy, angioplasty, and surgery. In general, patients with a stenosis greater than 50%, a translesional systolic pressure gradient greater than 15 mm Hg, and difficult-to-control hypertension and/or worsening renal insufficiency are candidates for renal revascularization. Percutaneous transluminal revascularization has evolved to become the preferred revascularization therapy because it is a less invasive and more cost-effective alternative to surgery and is associated with high technical success, as well as a low complication rate. The natural history of RAS is to progress over time, leading to renal artery occlusion, loss of renal mass, worsening of renal function, and, ultimately, end-stage renal disease. It is therefore important to aggressively screen, recognize, and treat the entity early in its course.
Rev Cardiovasc Med 2004
PMID:Current advances in the diagnosis and treatment of renal artery stenosis. 1558 Jan 59

Transcatheter closure of atrial septal defects (ASDs) is a safe and effective treatment. Over the past years, an increasing number of elderly patients (age > 60 years) have been admitted for transcatheter closure to prevent ongoing congestive heart failure from volume overload. However, recent data point to the risk of serious acute left ventricular dysfunction leading to pulmonary edema immediately after surgical or transcatheter ASD closure in some patients. In this study, we used a technique described before to recognize in advance patients at risk of left heart failure after ASD closure. Those patients at risk were then treated with preventive conditioning medication for 48-72 hr before definitive transcatheter ASD closure was performed. Fifty-nine patients aged over 60 years (range, 60-81.8 years; median, 68 years) were admitted to our institution for transcatheter closure of an atrial septal defect. All patients received evaluation of atrial pressures before and during temporary balloon occlusion of the ASD. Patients with left ventricular restriction due to increased mean atrial pressures (> 10 mm Hg) during ASD occlusion received anticongestive conditioning medication with i.v. dopamine, milrinone, and furosemide for 48-72 hr before definitive ASD closure with an Amplatzer septal occluder was performed. In 44 patients without any signs of left ventricular restriction, ASD closure was performed within the first session. Fifteen (25%) out of 59 patients showed left ventricular restriction. In the majority of patients with LV restriction, the mean left atrial pressures with occluded ASD were significantly decreased after 48-72 hr of conditioning medication. Definitive ASD closure was then performed in a second session. Only two patients received a fenestrated 32 mm Amplatzer occluder due to persistent increased atrial pressures > 10 mm Hg even after conditioning medication. There were no significant differences in shunt, device size, or defect size between the two groups. Balloon occlusion of atrial septal defects identifies patients with left ventricular restrictive physiology before ASD closure. Intravenous anticongestive conditioning medication seems to be highly effective in preventing congestive heart failure after interventional closure of an ASD in the elderly patient with a restrictive left ventricle.
Catheter Cardiovasc Interv 2005 Mar
PMID:Left ventricular conditioning in the elderly patient to prevent congestive heart failure after transcatheter closure of atrial septal defect. 1573 52

We report a repeated mitral valve replacement (re-do MVR) using the valve-on-valve technique for a degenerated bioprosthesis. A 49-year-old female, who had had a 29 mm Carpentier-Edwards mitral bioprosthesis for mitral regurgitation 20 years previously, was referred to our institution for dyspnea. She presented with pulmonary edema secondary to severe mitral bioprosthetic valve regurgitation. We replaced the degenerated mitral bioprosthesis with a 25 mm mechanical prosthesis using the valve-on-valve technique, as the struts of the bioprosthesis were embedded in the left ventricular myocardium. Removal of the bioprosthesis may be not only time-consuming but also complicated by cardiac rupture at the atrioventricular junction or the posterior left ventricular wall. The valve-on-valve technique is a simplified procedure that can avoid the potential complications of complete excision of the bioprosthesis. We believe this technique can be a useful strategy for patients with a degenerated mitral bioprosthesis.
Ann Thorac Cardiovasc Surg 2005 Apr
PMID:Re-do mitral valve replacement using the valve-on-valve technique: a case report. 1590 Feb 46


<< Previous 1 2 3 4 5 6 7 8 9 10