lisinopril and Hypertension--Pulmonary

The Fontan procedure is the final common pathway in the surgical palliation of many single ventricle heart defects. Mortality has improved but morbidity remains significant. Pleural effusions continue to present challenges after this operation and account for increased length of stay and increased time with draining tube thoracostomies. This review examines recent publications addressing this problem.. Four papers in 2008-2009 addressed effusions after the Fontan procedure. Off-pump Fontan procedures did not decrease time until chest tube removal. Pulmonary vascular compliance, derived from an electrical circuit model, predicted chest tube indwelling time. A retrospective study identified mean pulmonary artery pressure as a risk factor for effusions lasting more than 14 days after the Fontan procedure. One prospective, randomized trial evaluated the effects of lisinopril on pleural effusions after the Fontan procedure. There was no difference in the length of pleural drainage between the two groups.. Pleural effusions after the Fontan procedure continue to be a challenge. The cause is likely multifactorial and could explain why the literature has no clear message. One randomized, prospective trial suggests that fenestration reduces effusions. Many other reviews report no benefit to fenestration. Sildenafil after the Fontan procedure should be studied in a randomized, prospective fashion.

Topics: Antihypertensive Agents; Chest Tubes; Drainage; Fontan Procedure; Heart Defects, Congenital; Humans; Hypertension, Pulmonary; Lisinopril; Piperazines; Pleural Effusion; Postoperative Complications; Purines; Sildenafil Citrate; Sulfones; Vasodilator Agents

Total-body irradiation causes acute and delayed toxicity to hematopoietic, pulmonary, cardiac, gastrointestinal, renal, and other organ systems. Angiotensin-converting enzyme inhibitors mitigate many of the delayed injuries to these systems. The purpose of this study was to define echocardiographic features in rats at two times after irradiation, the first before lethal radiation pneumonitis (50 d) and the second after recovery from pneumonitis but before lethal radiation nephropathy (100 d), and to determine the actions of the angiotensin-converting enzyme inhibitor lisinopril. Four groups of female WAG/RijCmcr rats at 11-12 wk of age were studied: nonirradiated, nonirradiated plus lisinopril, 13-Gy partial-body irradiation sparing one hind leg (leg-out partial-body irradiation), and 13-Gy leg-out partial-body irradiation plus lisinopril. Lisinopril was started 7 d after radiation. Echocardiograms were obtained at 50 and 100 d, and cardiac histology was assessed after 100 d. Irradiation without lisinopril demonstrated echocardiographic transient pulmonary hypertension by 50 d which was largely resolved by 100 d in survivors. Irradiated rats given lisinopril showed no increase in pulmonary artery pressures at 50 d but exhibited left ventricular remodeling. By 100 d these rats showed some signs of pulmonary hypertension. Lisinopril alone had no impact on echocardiographic end points at either time point in nonirradiated rats. Mild increases in mast cells and fibrosis in the heart were observed after 100 d following 13-Gy leg-out partial-body irradiation. These data demonstrate irradiation-induced pulmonary hypertension which was reversed in survivors of pneumonitis. Lisinopril modified cardiovascular remodeling to enhance survival in this model from 41% to 86% (p = 0.0013).

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Echocardiography; Female; Hypertension, Pulmonary; Lisinopril; Myocardium; Radiation Injuries, Experimental; Radiation Pneumonitis; Rats; Ventricular Remodeling

The paper contains review of the role of endothelial dysfunction in heart failure in patients with combination of ischemic heart disease and chronic obstructive pulmonary disease and discussion of results of a study in which it was established that lisinopril (10 mg/day) caused attenuation of pulmonary hypertension, improvement of right ventricular systolic function and diastolic ventricular filling at the background of correction of vascular tone.

Topics: Angiotensin-Converting Enzyme Inhibitors; Drug Administration Schedule; Endothelium, Vascular; Female; Heart Failure; Humans; Hypertension, Pulmonary; Lisinopril; Male; Middle Aged; Myocardial Ischemia; Pulmonary Disease, Chronic Obstructive

to study the clinical and hemodynamic effects and safety of the ACE inhibitor dirotone and AT1-receptor antagonist losartan in secondary pulmonary hypertension (PH) in patients with chronic obstructive bronchitis (COB).. The time course of changes in hemodynamic parameters and diurnal BP profile in 48 patients with COB concurrent with Functional Class (FC) III-IV secondary PH, receiving 4-week therapy including dirotone and losartan.. The inclusion of dirotone or losartan into the combined therapy of patients with secondary pulmonary hypertension resulted in alleviated PH, caused positive changes in the right cardiac cavities, and normalized diurnal BP variables. Therapy with dirotone was effective in COB patients with the clinical signs of FC III PH only during its course use, that with losartan was beneficial in FC III and IV PH. The long-term outpatient use of losartan in individually adjusted doses produced pronounced beneficial clinical effects and led to significantly improved hemodynamic parameters.. The ACE inhibitor dirotone and the AT1-receptor antagonist losartan may be recommended for the correction of hemodynamic disorders in secondary PH in patients with COB.

Topics: Adult; Angiotensin-Converting Enzyme Inhibitors; Bronchitis, Chronic; Drug Administration Schedule; Drug Therapy, Combination; Female; Humans; Hypertension, Pulmonary; Lisinopril; Losartan; Male; Middle Aged