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

Holter recordings of subjects apparently free from cardiovascular disease have demonstrated a moderate sinusal and nodal depression during sleep. This depression does not seem to be sufficient to create overt cardiovascular disorders in apparently healthy subjects, but it may aggravate or even reveal an underlying disorder of rhythm or conduction in elderly people or in patients taking drugs that potentiate its effects. In sleep apnea syndrome prolonged episodes of apnea may produce a paroxysmal, then permanent increase in pulmonary arterial pressure, which may lead to right heart failure. These episodes also increase the pre- and after-load and decrease myocardial contractility, thus facilitating the occurrence of left ventricular failure, potentiated by systemic arterial hypertension, overweight or even coronary disease, all conditions that are often present in these subjects. Arterial hypertension is so frequent in sleep apnea syndrome that some authors advocate a systematic search for the syndrome by Holter recordings before the hypertension is pronounced "essential". All studies confirm the existence of rhythm and conduction disorders directly related to apneic episodes. These disorders decrease or regress after a well-conducted treatment of the sleep apnea syndrome. They are mainly of the "hypokinetic" type, created by depression of sinus activity and conduction pathways. Their frequency, their severity and, in particular, the risk of sudden death they carry seem to have been overestimated, especially since no evidence has ever been produced of a potentially lethal rhythm disorder occurring during sleep apnea. Nevertheless, there is no certainty that these patients are not at risk of sudden death related to their sleep apnea syndrome.
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PMID:[Cardiovascular disorders during sleep]. 214 78

We report the intensive care management of 23 children (age 3-15 years) following orthotopic heart (HT) and combined heart and lung transplantation (HLT) performed at our 2 institutes between February 1985 and August 1989. Cyclosporin A, azathioprine and steroids were given as routine immunosuppression, whilst anti-thymocyte globulin (ATG) was used for the first 3 post-operative days. Mean ventilation time was 24.6 h (range 4-74 h). Cardiovascular support comprised isoprenaline infusions in all patients (mean period 65.7 h) whilst dopamine and other inotropic agents were used less frequently. Sequential atrioventricular pacing was required more often in the HT patients (n = 9) than in the HLT patients (n = 4). Fluid input was restricted to maintain a plasma osmolality of 290-300 mosm/kg. There were 2 perioperative deaths both due to acute right heart failure. Other post-operative complications included: bleeding (n = 3); acute graft rejection (n = 4); infection (n = 3); systemic hypertension (n = 6); neurological abnormalities (n = 2); renal dysfunction (n = 6) and hyperglycaemia (n = 6).
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PMID:Intensive care management of children following heart and heart-lung transplantation. 226 10

Fenfluramine is a widely prescribed anorectic drug as adjuvant therapy for obesity. Pulmonary vascular hypertension after use of fenfluramine is rarely reported. We present a patient with pulmonary hypertension and right heart failure after treatment with fenfluramine. Pulmonary hypertension resolved after withdrawal of the drug.
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PMID:Pulmonary hypertension and fenfluramine. 237 56

Pulmonary embolism can produce severe cardiopulmonary dysfunction characterized by pulmonary artery hypertension, right ventricular failure, and hypoxemia. The search for the source of a pulmonary embolus, by exploration of the veins of the lower limbs and the inferior vena cava should be systematically carried out in all cases of pulmonary embolus which are not immediately life-threatening to the patient. The treatment of deep vein thrombosis associated with pulmonary embolism with thrombolytic agents has been proposed and utilized for approximately 20 years. Although superior results have been claimed with thrombolytic agents, the use of this type of treatment remains limited to massive or sub-massive pulmonary embolism. Fibrinolytic agents with high specificity for fibrin in the thrombi and little systemic activation of the fibrinolytic system have been developed and tested in preliminary clinical trials of patients with acute pulmonary embolism. The largest published experience available has been with recombinant tissue plasminogen activator (rtPA). The acylated streptokinase-plasminogen complex (APSAC) and pro-urokinase also gave promising results. All these agents were accompanied by unexpectedly high incidence of systemic activation of the fibrinolytic system and by hemorrhagic complications with frequencies similar to those that follows the use of first generation products (urokinase and streptokinase). Hence, their superior clinical efficacy must be clearly proven before they are substituted for a more widely available and less expensive drug, such as streptokinase.
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PMID:Pathogenesis and management of acute pulmonary embolism. 251 49

Unlike the left ventricle, the right ventricle is a thin-walled, low-pressure, volume-displacement pump that ensures adequacy of left ventricular filling and maintains a low pressure in the venous system. In healthy human subjects, there is no burden for right ventricular systolic emptying, because normal pulmonary vessels have a low impedance and show a passive recruitment when cardiac output increases. However, under a pathological condition like right-sided heart failure, the right ventricle may exert profound influences on the circulatory state. Right-sided heart failure most often results from primary or secondary pulmonary arterial hypertension. Pharmacologic vasodilation of the hypertensive pulmonary vascular bed is an ideal therapy for right-sided heart failure. The bipyridine derivative amrinone has positive inotropic and direct vasodilator properties, and therefore seems suitable for the therapy of right ventricular dysfunction accompanied by pulmonary arterial hypertension. In one study, 12 patients with right ventricular failure due to mitral valve stenosis were evaluated, and it was found that amrinone increased cardiac output by 25% and decreased pulmonary artery pressure by 30% to 50%. In a second study, the hemodynamic properties of amrinone versus sodium nitroprusside were compared in patients with aortic or mitral valve failure (n = 17), when both agents lowered systemic vascular resistance equally. Pulmonary vascular resistance decreased significantly (25%) only in the amrinone group.
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PMID:Effects of amrinone on the right side of the heart. 252 Oct 50

Chronic obstructive lung diseases (COLD) are very often complicated by pulmonary arterial hypertension and right heart failure. Several drugs including nitrates have been used to counteract this type of hypertension. Molsidomine (M) is a recent nitrates-like drug acting for a longer time than the classical nitrates. Our aim was to investigate whether M could significantly lower pulmonary arterial hypertension of patients suffering from COLD. Ten male patients were investigated before and after intake of 4.0 mg M given sublingually. Ventilatory and cardiocirculatory indices were measured at rest and during a 30 and a 50 watts exercise. During exercise, M significantly lowers pulmonary arterial pressure and pulmonary vascular resistance without detrimental effect on arterial blood gases. M seems to be a promising drug to counteract the pulmonary hypertension of patients with COLD.
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PMID:Acute effect of molsidomine on pulmonary circulation of patients with chronic obstructive pulmonary disease. 260 19

In chronic obstructive bronchopneumopathies (COBP), pulmonary artery hypertension (PAH) is usually mild but may markedly intensify during episodes of acute respiratory failure, muscular exercise, and sleep, PAH may, even if of low level, lead to right heart failure. The prognostic value of PAH and its degree in COBP patients has been well established by a number of recent studies. Chronologic changes in pulmonary artery pressure (PAP) tend to be minimal in the majority of COBP patients (of the order of +0.5-0.6 mm Hg/year in most studies). However, in a minority of patients (about 30%) pulmonary hypertension worsens seriously due to progressive deterioration of arterial blood gases. Longterm oxygen therapy (LOT) for 16 h/day rarely serves to normalize PAP but may reverse the progress of pulmonary hypertension, particularly in patients with progressive aggravation thereof. Recent studies have made it clear that LOT has beneficial hemodynamic effects in a relatively large percentage of COBP patients with PAH.
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PMID:[Development of pulmonary arterial hypertension in chronic obstructive bronchopneumopathies]. 269 44

Ten patients underwent mitral valve re-replacement for the third to sixth time through a right thoracotomy using one-lung anesthesia, femorofemoral bypass, profound systemic hypothermia, and low-flow perfusion without aortic cross-clamping or cardioplegia. The indications for this approach were previous mediastinitis, severe right ventricular hypertension with multiple previous sternotomies, intact coronary artery bypass graft, or previous aortic valve replacement. There was 1 operative death, which was due to end-stage pulmonary hypertension and intractable right heart failure. Blood loss was minimal, and there was no major postoperative morbidity in the 9 surviving patients except for supraventricular arrhythmias.
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PMID:Right thoracotomy, femorofemoral bypass, and deep hypothermia for re-replacement of the mitral valve. 276 4

In 106 patients suffering from acute respiratory failure of different severity 157 bedside balloon occlusion pulmonary angiographic studies have been performed through a pulmonary artery catheter to assess the frequency and extent of intravascular occlusive disease. The vascular alterations in acute respiratory failure impair the prognosis essentially. The decreasing pulmonary vascular cross-section causes a greater pulmonary vascular resistance and consecutive pulmonary artery hypertension and finally right heart failure. In 33% of patients multiple thrombosis and in 15.1% singularly pulmonary artery filling defects could be shown. In 21.7% a decreased background opacification caused by extensive microthrombosis was present. Only in 30.2% the angiography was interpreted as normal. The mortality rate was significant higher in patients with multiple macro- and microthrombosis (82.9% respectively 52.2%) compared to patients with singular pulmonary artery filling defects and normal angiography (37.5% respectively 28.1%). The angiographic result was further correlated with the severity of the acute respiratory failure, the haemodynamic and haemostasiologic data, the degree of consolidation in the chest-X-ray and the post mortem angiographic studies.
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PMID:[Incidence and prognostic significance of pulmonary artery thromboses in patients with acute respiratory failure: a study of 106 patients using bilateral pulmonary balloon occlusion angiography]. 280 May 53

Drugs with pharmacological activity limited to the pulmonary circulation are not at present available. Serotonin antagonists, specific thromboxane A2 inhibitors and prostacyclin may offer new possibilities for the treatment of certain forms of pulmonary arterial hypertension (PAH), but their clinical efficacy remains to be evaluated. Vasodilators simultaneously influence the pulmonary and systemic vascular resistances, and their overall hemodynamic effects in patients with PAH are therefore unpredictable. Therapeutic trials with such drugs should be closely monitored to avoid serious adverse reactions. Oral administration of beta-adrenergic agents, such as salbutamol or terbutaline, is preferable to digoxin in the treatment of patients with right ventricular failure due to chronic obstructive bronchitis. Right ventricular failure following massive pulmonary embolism may be aggravated by reduced blood flow through the right coronary artery. Increase of aortic perfusion pressure (e.g. noradrenaline) should be considered as a therapeutic measure in patients with arterial hypotension.
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PMID:[Pharmacology of the pulmonary circulation]. 286 81


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