Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report on a case of acute non-cardiogenic negative-pressure pulmonary edema developed during an ablation procedure of an accessory pathway in a patient with no structural heart disease. That potentially serious complication has not been previously reported during an interventional cardiology procedure.
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PMID:Negative pressure pulmonary edema complicating an electrophysiological study. 1944 50

Protein kinase (PK)Calpha, PKCbeta, and PKCgamma comprise the conventional PKC isoform subfamily, which is thought to regulate cardiac disease responsiveness. Indeed, mice lacking the gene for PKCalpha show enhanced cardiac contractility and reduced susceptibility to heart failure. Recent data also suggest that inhibition of conventional PKC isoforms with Ro-32-0432 or Ro-31-8220 enhances heart function and antagonizes failure, although the isoform responsible for these effects is unknown. Here, we investigated mice lacking PKCalpha, PKCbeta, and PKCgamma for effects on cardiac contractility and heart failure susceptibility. PKCalpha(-/-) mice, but not PKCbetagamma(-/-) mice, showed increased cardiac contractility, myocyte cellular contractility, Ca(2+) transients, and sarcoplasmic reticulum Ca(2+) load. PKCalpha(-/-) mice were less susceptible to heart failure following long-term pressure-overload stimulation or 4 weeks after myocardial infarction injury, whereas PKCbetagamma(-/-) mice showed more severe failure. Infusion of ruboxistaurin (LY333531), an orally available PKCalpha/beta/gamma inhibitor, increased cardiac contractility in wild-type and PKCbetagamma(-/-) mice, but not in PKCalpha(-/-) mice. More importantly, ruboxistaurin prevented death in wild-type mice throughout 10 weeks of pressure-overload stimulation, reduced ventricular dilation, enhanced ventricular performance, reduced fibrosis, and reduced pulmonary edema comparable to or better than metoprolol treatment. Ruboxistaurin was also administered to PKCbetagamma(-/-) mice subjected to pressure overload, resulting in less death and heart failure, implicating PKCalpha as the primary target of this drug in mitigating heart disease. As an aside, PKCalphabetagamma triple-null mice showed no defect in cardiac hypertrophy following pressure-overload stimulation. In conclusion, PKCalpha functions distinctly from PKCbeta and PKCgamma in regulating cardiac contractility and heart failure, and broad-acting PKC inhibitors such as ruboxistaurin could represent a novel therapeutic approach in treating human heart failure.
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PMID:Protein kinase C{alpha}, but not PKC{beta} or PKC{gamma}, regulates contractility and heart failure susceptibility: implications for ruboxistaurin as a novel therapeutic approach. 1955 21

Left heart disease is the most common cause of pulmonary hypertension. Increased left-sided filling pressure leads to passive postcapillary venous hypertension. In some patients, pulmonary vasoconstriction and vascular remodeling may lead to a further increase in pulmonary pressure. When precapillary hypertension component is associated to left heart failure, the elevation of pulmonary pressure is out of proportion with left atrial pressure: transpulmonary gradient greater than 12 mmHg (mean pulmonary pressure -- mean capillary pressure) and pulmonary vascular resistance greater than three Wood units. Precapillary pulmonary hypertension is common in severe systolic heart failure. Before cardiac transplantation, increased pulmonary vascular resistance greater than 3,5 Wood units are reported in 19 to 35% of patients. In those patients vasoreactivity tests are performed with inotropic and/or systemic and/or pulmonary agents to determine the risk of right heart failure after transplantation. There is no pulmonary vascular resistance level above which transplantation is contraindicated. Cardiac assistance may be used before and after transplantation when pulmonary hypertension is severe and not reversible with conventional treatment and/or pulmonary vasodilators. The contribution of precapillary PH in diastolic heart failure is not known but can be significant and lead to disproportionate PH particularly in elderly. The precapillary component of pulmonary hypertension could be a therapeutic target for specific pulmonary vasodilators. Until now pharmacological trials has been disappointing and those medications can be dangerous because of increasing blood flow to the pulmonary capillaries with a risk of pulmonary edema when left sided pressure are still elevated.
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PMID:[Pulmonary hypertension and heart failure: the role of pulmonary vasculature]. 1981 18

Valvular heart diseases have adverse effects on hemodynamic condition in the parturients during pregnancy. Cesarean section with an opioid based general anesthesia has been used to alleviate these deleterious effects. We hereby describe the effective application of remifentanil, for cesarean section under general anesthesia, in a 30 yr. old primigravida suffering of severe multivalvular heart disease and pulmonary hypertension presenting with pulmonary edema who was in active labor and without neonatal respiratory depression.
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PMID:The use of remifentanil in general anesthesia for cesarean section in a parturient with severe mitral stenosis and pulmonary edema. 2039 60

Patients who had no heart disease had T-wave inversion and prolongation of the QT interval in electrocardiogram after Subarachnoid hemorrhage (SAH), which was reported 70years before. Cardiac complications, including focal myocytolysis, electrocardiographic changes, arrhythmias and left ventricular wall motion abnormalities and pulmonary edema. The autonomic and cardiovascular effects of SAH, however, are modulated by concomitant factors such as pre-existent cardiac diseases, electrolyte disorders and, probably, by genetic alterations in the ionic control of myocyte repolarization. Although beta-blockers have been reported to prevent myocardial damage following SAH, adequate clinical trials are lacking, and the widespread use of these drugs in acute cerebrovascular disease is not supported by evidence. Cardiac injury occurs frequently after SAH, and the most widely investigated form of neurocardiogenic injury.
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PMID:Cardiac damage after subarachnoid hemorrhage. 2111 42

Cardiac and pulmonary pathophysiologies are closely interdependent, which makes the management of patients with congenital heart disease (CHD) all the more complex. Pulmonary complications of CHD can be structural due to compression causing airway malacia or atelectasis of the lung. Surgical repair of CHD can also result in structural trauma to the respiratory system, e.g., chylothorax, subglottic stenosis, or diaphragmatic paralysis. Disruption of the Starling forces in the pulmonary vascular system in certain types of CHD lead to alveolar-capillary membrane damage and pulmonary oedema. This in turn results in poorly compliant lungs with a restrictive lung function pattern that can deteriorate to cause hypoxemia. The circulation post single ventricle palliative surgery (the so called "Fontan circulation") poses a unique spectrum of pulmonary pathophysiology with restrictive lung function and a low pulmonary blood flow state that predisposes to thromboembolic complications and plastic bronchitis. As the population of patients surviving post CHD repair increases, the incidence of pulmonary complications has also increased and presents a unique cohort in both the paediatric and adult clinics.
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PMID:Pulmonary complications of congenital heart disease. 2220 88

Diving-related pulmonary oedema (DRPO) is an uncommon and incompletely understood phenomenon. Pulmonary oedema has been rarely documented in shallow water. It is also associated with cold water and exertion and has been seen in swimmers as well as divers with no underlying heart disease. We describe an otherwise well 69-year-old lady who developed diving-related pulmonary oedema on her second and third dives in a shallow, heated pool. Follow-up echocardiogram revealed moderate global left ventricular dysfunction with an ejection fraction of 37%. There was a history of alcohol consumption of half a bottle of wine per day, which combined with the echocardiographic findings led to the diagnosis of alcoholic cardiomyopathy. We believe this not only to be the oldest patient with a documented case of DRPO but also the first report where it has clearly unmasked clinically significant underlying heart disease.
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PMID:Diving-related pulmonary oedema as an unusual presentation of alcoholic cardiomyopathy. 2269 9

Transfusion-related acute lung injury (TRALI) is an underdiagnosed and underreported syndrome which by itself is the third leading cause of transfusion-related mortality. The incidence of TRALI is reported to be 1 in 2000 to 5000 transfusions. When combined with uncontrollable bleeding, survival is unachievable. We report the case of a 25-year-old man, who underwent open heart surgery as an infant to correct his congenital heart disease in association with right pulmonary artery atresia. He presented with hemoptysis secondary to aspergilloma and required a pneumonectomy of the nonfunctional right lung. During pneumolysis, significant bleeding occurred from the superior vena cava. The patient required a blood transfusion and was placed on cardiopulmonary bypass to control the bleeding. Simultaneous occurrence of severe pulmonary edema and retroperitoneal bleeding were noted. Approximately 8 L of frothy edema fluid were drained from the only functional left lung starting ~15 minutes after the transfusion and lasting for several hours until the end of the case. It most likely represented TRALI syndrome. Increasing abdominal girth and poor volume return to the pump were consistent with and pathognomonic for retroperitoneal bleeding. Though primary surgical bleeding in the chest was controlled successfully and a pneumonectomy performed without further difficulty, we were unable to separate the patient from cardiopulmonary bypass due to the inability to oxygenate. As a result, we could not reverse the anti-coagulation which potentially exacerbated the retroperitoneal bleeding. After multiple unsuccessful attempts the patient succumbed. This ill-fated case demonstrates the quandary of obtaining vascular access for emergency cardiopulmonary bypass while in the right thoracotomy position. It may be beneficial to have both the femoral artery and vein cannulated before positioning a patient in a lateral decubitus position. In addition, early direct access to the right atrium may obviate a need for femoral venous cannulation. Also, adult extracorporeal membrane oxygenation may be indicated if faced with such a severe pulmonary edema without ongoing hemorrhage.
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PMID:TRALI Syndrome Complicated by Retroperitoneal Bleeding. 2294 33

Cardiac asthma has been defined as wheezing, coughing and orthopnea due to congestive heart failure. The clinical distinction between bronchial asthma and cardiac asthma can be straight forward, except in patients with chronic lung disease coexisting with left heart disease. Pulmonary edema and pulmonary vascular congestion have been thought to be the primary causes of cardiac asthma but most patients have a poor response to diuretics. There appears to be limited effectiveness of classical asthma medications like bronchodilators or corticosteroids in treating cardiac asthma. Evidence suggests that circulating inflammatory factors and tissue growth factors also lead to airway obstruction suggesting the possibility of developing novel therapies.
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PMID:Cardiac asthma: new insights into an old disease. 2323 54

Pulmonary edema may develop secondary to several cardiogenic and noncardiogenic conditions. Cardiogenic pulmonary edema (CPE) is associated with heart disease, an elevation in left atrial pressure, and an increase in pulmonary venous and capillary pressures. In contrast, noncardiogenic pulmonary edema (NCPE) can occur without pathologic cardiac disease and an elevation in left atrial pressure. NCPE has been associated with an increase in capillary membrane permeability with or without an increase in hydrostatic pressure. Signalment, history, and thoracic radiography may help distinguish NCPE from CPE. Some types of NCPE are self-limiting, and treatment may be largely supportive; others may require pharmacologic intervention and advanced respiratory support.
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PMID:Noncardiogenic pulmonary edema. 2353 87


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