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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of heart failure in octogenarians is high and its diagnosis not always easy. In many cases it is made by excess or by omission. Obtaining a history is often difficult. Signs may be masked, false or indicative of another disease process. Dyspnea, edema of the lower limbs and crepitations are relatively non-specific. Jugular distension, tender hepatomegaly and a diastolic gallop are much more valuable. Diagnosis of the underlying etiology also raises problems. While hypertension is commonplace and easy to identify, ischemic heart disease is common and often missed. Tight aortic stenosis must be identified since its treatment is surgical. Hypertrophic cardiomyopathy is often an echocardiographic discovery. Post-embolic chronic cor pulmonale, or secondary to chronic obstructive lung disease, must always be considered in the presence of right heart failure without hypertension or chest pain. Appropriate treatment is dependent upon accurate diagnosis.
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PMID:[Difficulties in the diagnosis of cardiac insufficiency in octogenarians]. 782 52

In chronic respiratory diseases, especially chronic obstructive pulmonary disease (COPD) pulmonary arterial hypertension is generally mild to moderate and the necessity for treating it can, therefore, be questioned. In fact, pulmonary hypertension, even when modest, may worsen markedly during acute episodes, exercise and sleep. These acute increases in mean pulmonary artery pressure (PAP) could contribute to the development of right heart failure. Therefore, the medical treatment of pulmonary hypertension is justified. There are, at the present time, no selective pulmonary vasodilators, with the exception of inhaled nitric oxide. Indeed, vasodilators appear less effective in COPD compared to primary pulmonary hypertension. Thus, there is, at present, no justification for the long-term use of vasodilators in COPD patients. Long-term oxygen therapy (LTOT) attenuates and sometimes reverses the progression of pulmonary hypertension, although the condition rarely returns to normal. We do not know whether the structural changes of the pulmonary vasculature in COPD patients are potentially reversible with LTOT. The longer the daily duration of LTOT the better are the haemodynamic results. At present, LTOT remains the best treatment for pulmonary hypertension in COPD patient. In the future, treatment of this condition in COPD patients could combine LTOT and specific vasodilators.
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PMID:Medical treatment of pulmonary hypertension in chronic lung disease. 814 14

A case of multiple focal nodular hyperplasia (FNH) of the liver associated with noncirrhotic portal hypertension and later complicated by pulmonary arterial hypertension leading to death from right heart failure is reported. In retrospect, the portal hypertension diagnosed in early life was most likely due to a congenital hypoplasia of portal vein branches and multiple FNH, a hyperplastic response of the liver parenchyma in association with anomalies of hepatic arterial branches as found within the lesions. This case may represent a form of multiple FNH syndrome restricted to the liver, because neither extrahepatic vascular malformation nor brain tumor was identified at autopsy. The FNH lesions had considerably expanded over the years, and the severe sinusoidal congestion due to chronic right-sided heart failure with subsequent prolonged parenchymal exposure to blood-borne hepatotrophic factors is a likely explanation for both the massive enlargement of FNH lesions and the nodular regenerative hyperplasia observed in the intervening parenchyma.
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PMID:Nodular transformation of the liver associated with portal and pulmonary arterial hypertension. 822 77

A 72-year-old female, who had received medication for hypertension and angina pectoris was hospitalized with complaining of an abrupt dyspnea. Roentgenogram of the chest revealed no abnormal findings except cardiac enlargement. An electrocardiogram showed overloading of the right ventricle. Arterial blood gas analysis of room air showed 55.4 mmHg of PaO2, 25.5 mmHg of PaCO2 and 7.30 of PH, respectively. Acute and massive pulmonary embolism was diagnosed by an emergent pulmonary arteriography. Despite intensive treatment such as infusion of urokinase and heparin for four days, thrombus was still detected in the left main pulmonary artery by a transesophageal echocardiography. By the result of ineffective conservative therapy, embolectomy was performed under cardiopulmonary bypass. However mechanical respiratory support was required for a long time due to the right heart failure, she is doing well for a year after the operation.
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PMID:[Acute massive pulmonary embolism--report of a case]. 845 37

Pulmonary artery (PA) hypertension in transplant recipients increases mortality from right heart failure following heart transplantation. We examined the impact of long-term medical therapy on the severity of PA hypertension in patients with end-stage congestive heart failure on a transplant waiting list. The initial and final, quarterly right heart catheterization data on 60 patients (50 men, aged 50 +/- 9 years, New York Heart Association class III to IV) awaiting heart transplantation were analyzed and the patients divided into 2 groups: group A, those with persistent elevated systolic PA pressures throughout the 10-month follow-up (n = 31 of 60), and group B, those who had any decrease in systolic PA pressure during that period (n = 29 of 60). Group A had no change in hemodynamics. Group B had a significant decrease( +/- SD) in right atrial (11 +/- 7 to 5 +/- 4 mm Hg), PA (57 +/- 11 to 37 +/- 11 mm Hg), and PA wedge (25 +/- 9 to 14 +/- 7 mm Hg) pressures, with increases in cardiac output (3.8 +/- 0.9 to 4.7 +/- 1.1 L/min) and ejection fraction (18 +/- 6% to 27 +/- 11%) (p < 0.05). The combined end point of transplant or death occurred in 28 of 31 patients (90%) in group A versus 14 of 29 (50%) in group B (p = 0.0004). Ischemic etiology was present in 71 % of patients in group A versus 68% with idiopathic dilated cardiomyopathy in group B (p = 0.003). The reversibility of PA hypertension rather than its initial severity is predictive of patient clinical outcome. Idiopathic, as opposed to ischemic, cardiomyopathy responds better to medical therapy.
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PMID:Impact of medical therapy on pulmonary hypertension in patients with congestive heart failure awaiting cardiac transplantation. 875 90

Patients with obstructive sleep apnea demonstrate both acute and chronic hemodynamic changes attributable to their disease. Acutely, these patients experience repetitive nocturnal hemodynamic oscillations. Sudden increases in heart rate and arterial pressure occur in association with decreases in left ventricular stroke volume immediately following apnea termination. These hemodynamic changes are likely attributable primarily to the effects of oxygen desaturation and arousal, an abrupt change in state. These acute changes occur against a background of altered cardiovascular control. Patients with sleep apnea, even when sleeping without obstructions, fail to display the normal nocturnal decline in arterial pressure of 10-15% from the waking value. The absence of a nocturnal decline may have chronic consequences, such as development of left ventricular hypertrophy. Another chronic hemodynamic consequence of sleep apnea may be sustained diurnal hypertension. Epidemiologic studies suggest individuals with sleep disordered breathing are at greater risk of daytime hypertension, even after controlling for other risk factors. Although sleep apnea may contribute to pulmonary, as well as systemic hypertension, sleep apnea alone does not appear to be a cause of decompensated right heart failure. Although knowledge of the hemodynamic consequences of sleep apnea has grown in recent years, much remains to be learned.
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PMID:Hemodynamic consequences of obstructive sleep apnea. 884 30

A 52-year-old male for CABG developed a severe right heart failure, because of the direct injury to the right ventricular wall, after cardiopulmonary bypass. The volume loading therapy could not improve the cardiac function, then we used an infusion of low-dose prostaglandin E1 (0.02-0.04 micrograms.kg-1.min-1) for the acute right heart failure with increased pulmonary vascular resistance. After continuous infusion of this dose, the pulmonary vascular resistance decreased quickly, the right ventricular ejection fraction increased, and the stroke volume index also improved. These hemodynamic changes are the result of the potent vasodilating effect of PGE1, that especially could decrease selectively the pulmonary vascular resistance, and increase the preload of the left ventricle. This dose of PGE1, did not cause a severe systemic hypertension that is a serious complication during vasodilating therapy with any vasoactive drugs. In the present case, we speculated that the low-dose PGE1, is effective to improve the right ventricular function during the acute right heart failure which resulted from the intrinsic right ventricular dysfunction.
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PMID:[Prostaglandin E1 at low-doses improved right ventricular ejection fraction in anesthetic management for CABG]. 893 28

An hydatid cyst of the left lobe of the liver, associated with right heart failure, was diagnosed in a 61-year-old man presenting with dyspnoea. Doppler echocardiography combined with cardiac catheterization demonstrated the presence of pulmonary precapillary hypertension. Pulmonary perfusion scintigraphy with Technetium-labelled albumin microspheres demonstrated multiple pulmonary embolisms, leading to a diagnosis of postembolic chronic cor pulmonale. Due to the absence of thrombophlebitis and ultrasound signs of an intracaval hydatid membrane, floating at the level of the cyst of the left lobe of the liver, the diagnosis of parasitic postembolic chronic heart pulmonale, due to fistulization of an hepatic hydatid cyst into the inferior vena cava, was established. Only chemotherapy was proposed in this patient due to dissemination of the hydatid material in the lungs.
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PMID:[Chronic cor pulmonale caused by hydatid embolism complicating hepatic hydatid cyst]. 929 92

The symptoms of amyloidosis depend on the type of precursor, the amount of deposits and their location. In systemic amyloidosis almost every organ may be involved. Cardiac involvement is severe, especially in AL amyloidosis, responsible for restrictive cardiomyopathy with right ventricular failure, leading rapidly to death. Renal amyloid deposition causes nephrotic syndrome with hypertension and renal failure. Neurological complications include peripheral neuropathy with dysautonomia cerebral involvement (dementia, cerebral haemorrhages). Arterial deposits are common in systemic senile amyloidosis, and may cause ischaemia. Osteo-articular damage is mainly seen in patients on long-term haemodialysis. Liver enlargement is often the only manifestation of hepatic amyloidosis. Digestive tract involvement includes macroglossia deposits in salivary glands and disturbances in gastrointestinal motility. Pulmonary amyloidosis causes nodular or interstitial infiltrates. Cutaneous lesions are various. Localized amyloidoses include goiter, breast and vesical involvement which can be difficult to differentiate from neoplasm, as well as ocular amyloidosis mimicking posterior uveitis.
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PMID:[Localizations and consequences]. 945

The role of endothelium in vascular relaxation is linked to the existence of endothelium derived relaxing factors (EDRF) known since 1980. In 1987, nitric oxide (NO) was identified as one of these factors. NO acts in many physiologic and pathophysiologic events. Atmospheric NO is a pollutant. Inhaled NO allows selective pulmonary vasodilation and is used to treat pulmonary artery hypertension (PAH). As inhaled NO is inactivated immediately in the blood by linking to haemoglobin, systemic vasodilation does not occur and right ventricular coronary perfusion pressure does not decrease. This is particularly important in the treatment of right ventricular failure due to PAH following cardiothoracic surgery. In patients with an acute respiratory distress syndrome (ARDS), inhaled NO improves the perfusion of adequately ventilated pulmonary territories. Very low concentrations of NO, such as two parts per million, decrease intrapulmonary venous admixture and may reverse hypoxaemia. However its long term benefits in ARDS must be assessed more accurately with multicentre controlled studies. Inhaled NO also improves refractory hypoxaemia in neonates. Its bronchodilatory effect, demonstrated experimentally, does not occur in acute obstructive bronchopulmonatory disease. The toxicity of NO, and overall of its oxidated derivative NO2 requires precise conditions of administration and close monitoring of inhaled fractions. In that case, the risk of NO toxicity seems very low when compared to its therapeutic benefits in selected patients.
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PMID:[Inhaled nitric oxide in anesthesia and intensive care]. 968 93


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