Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to evaluate which parameter of right ventricular (RV) echocardiographic best mirrors the clinical status of patients with pulmonary arterial hypertension. Patients with pulmonary arterial hypertension on epoprostenol therapy were identified via hospital registry. Twenty patients, (16 females, 4 males) were included in the study, 9 with primary pulmonary hypertension and 11 with other diseases. Echocardiograms before therapy and at 22.7 (+/-9.3) months into therapy were compared. The right ventricular myocardial performance index (RVMPI) was measured as the sum of the isometric contraction time and the isometric relaxation time divided by right ventricular ejection time. Other measures included peak tricuspid regurgitation jet velocity (TRV), pulmonary artery systolic pressure (PASP), pulmonary valve velocity time integral (PVVTI), PASP/PVVTI (as an index of total pulmonary resistance) and symptoms by New York Heart Association (NYHA) functional class. Echo parameters of right ventricular function were analyzed in patients, before and during therapy. There was significant improvement of NYHA class in patients following epoprostenol therapy (P < 0.0001). Peak tricuspid regurgitant jet velocity (pre 4.2 +/- 0.6 m/sec, post 3.8 +/- 0.7 m/sec, P = 0.02) and PASP/PVVTI (pre 6.7 +/- 3.3 mmHg/m per second, post 4.8 +/- 2.2 mmHg/m per second, P < 0.0001) were significantly improved during treatment. RVMPI did not improve (pre 0.6 +/- 0.3, post 0.6 +/- 0.3, P = 0.54). Changes in NYHA class did not correlate with changes in RVMPI (P = 0.33) or changes in PASP/PVVTI (P = 0.58). Despite significant improvements in TRV, PASP/PVVTI, and NYHA class, there was no significant change in RVMPI on epoprostenol therapy. Changes in right ventricular indices were not correlated with changes in NYHA class.
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PMID:Correlation between right ventricular indices and clinical improvement in epoprostenol treated pulmonary hypertension patients. 1590 Dec 87

Primary pulmonary arterial hypertension (PPH) is a rare disease of undetermined origin and fatal prognosis. A better prognosis is associated with at least 20% reduction of either pulmonary artery pressure or pulmonary vascular resistance ("responders") in acute vasodilatory trials. Prostacycline (PGI2) or nitric oxide (NO) administration promises valuable results. NO is one of the most powerful vasodilating agents, endogenously produced by endothelial cells. It migrates from these cells to smooth muscle cells and stimulates production of cGMP, that induces smooth muscle relaxation. cGMP is hydrolyzed by 5-phopshodiesterase (PDE-5). Several papers documenting hypotensive effect in pulmonary circulation of specific PDE5 inhibitor--sildenafil (Viagra--Pfizer) have been published recently. We present a case report of a 26 year old female patient with PPH--"nonresponder" in a trial with NO--and NO responder after sildenafil administration. Initial values were: mean pulmonary artery pressure (mPAP) was 58 mmHg, pulmonary vascular resistance was 10.9 Wood's units. mPAP and PVR during NO inhalation (40 ppm) decrease from 62 to 54 mmHg and from 11.4 to 10.3 Wood's units, respectively. Measurements performed 60 minutes after 50 mg of sildenafil orally disclosed a 19% reduction of mPAP and 21% reduction of PVR. NO inhalation caused further decrease of both parameters: mPAP was decreased for additional 28% and PVR for additional 36% in comparison to initial results. Neither peripheral hypotension nor other side effects were observed. A month-long administration of sildenafil in a dose 2 x 25 mg daily reduced mPAP and PVR to values reported for the acute trial. Physical capability improved also. It was assessed as increased distance in a six-minute-walk test (280 vs. 400 m in the first week of treatment, and 330 m in a fourth week of treatment). Echocardiography showed moderate decrease of right ventricle and right atrium diameters, along with decrease of the degree of relative tricuspid regurgitation with unchanged maximal velocity of regurgitant wave. Specific PDE-5 inhibitors might be an attractive alternative in the treatment of pulmonary hypertension in case the above noted observations are confirmed.
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PMID:[Sildenafil reduces pressure and pulmonary resistance and increases susceptibility of pulmonary arteries to nitric oxide in primary pulmonary arterial hypertension]. 1609 62

The principles of Fontan conversion with arrhythmia surgery are to restore the cardiac anatomy by converting the original atriopulmonary connection to a total cavopulmonary artery extracardiac connection and treat the underlying atrial arrhythmias. Successful outcomes of this procedure are dependent on a thorough understanding of several factors: the patient's fundamental diagnosis of single-ventricle anatomy, the resultant cardiac configuration from the original atriopulmonary Fontan connection, right atrial dilatation that leads to atrial flutter or fibrillation, and associated congenital cardiac anomalies. The purpose of this article is to present some of the more challenging anatomic and electrophysiologic problems we have encountered with Fontan conversion and arrhythmia surgery and the innovative solutions we have used to treat them. The cases reviewed herein include: takedown of a Bjork-Fontan modification, right ventricular hypertension and tricuspid regurgitation after atriopulmonary Fontan for pulmonary atresia and intact ventricular septum, takedown of atrioventricular valve isolation patch for right-sided maze procedure, resultant hemodynamic considerations leading to intraoperative pulmonary vein stenosis after Fontan conversion, unwanted inferior vena cava retraction during the extracardiac connection, right atrial cannulation in the presence of a right atrial clot, distended left superior vena cava causing left pulmonary vein stenosis, dropped atrial septum, and the modified right-sided maze procedure for various single-ventricle pathology. Since 1994 we have performed Fontan conversion with arrhythmia surgery on 109 patients with a 0.9% mortality rate. We attribute our program's success in no small measure to the strong collaborative efforts of the cardiothoracic surgery and cardiology teams.
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PMID:Evolving anatomic and electrophysiologic considerations associated with Fontan conversion. 1743 5

Hereditary hemorrhagic telangiectasia (HHT) or Rendu-Osler-Weber disease is a genetic disorder with autosomal dominance and variable penetrance, characterized by epistaxis, telangiectasia and visceral manifestations of the disease. The estimated minimal prevalence is 1/10,000 inhabitants. The diagnosis is established on clinical criteria, and may be further confirmed by the identification of causative mutations in either the ENG or the ACVRL1 gene coding for endoglin and ALK1, respectively. Pulmonary vascular manifestations of HHT include pulmonary arteriovenous malformations (PAVMs; especially in patients with ENG mutations) and less frequently pulmonary hypertension (especially in patients with ACVRL1 mutations). In 15-33% of patients with HHT, PAVMs consist of abnormal communications between pulmonary arteries and pulmonary veins, causing right-to-left shunting, and thus, frequently hypoxemia and dyspnea on exertion, although PAVMs may remain asymptomatic and frequently undiagnosed unless complications occur. PAVMs result in severe and frequent complications often at a young age, which may reveal the diagnosis, e.g. transient ischemic attack and cerebral stroke (10-19% of patients), systemic severe infections and abscesses (including cerebral abscess in 5-19% of patients), and rarely massive hemoptysis or hemothorax. Infections in HHT are related to the right-to-left shunting that bypasses the pulmonary capillaries and facilitates the passage of septic or aseptic emboli into the systemic and especially cerebral circulation, and potentially to minor defects in innate immunity. Treatment of PAVMs based on transcatheter coil vaso-occlusion of the feeding artery significantly decreases right-to-left shunting, hypoxemia and dyspnea on exertion, and reduces the risk of systemic complications. Long-term follow-up is warranted after transcatheter vaso-occlusion of PAVMs due to frequent recanalization of treated PAVMs and development or growth of untreated PAVMs. Patients with HHT should be informed of the risk of PAVM and potentially severe complications occurring in heretofore asymptomatic subjects. All adult patients with HHT should be proposed systematic screening for PAVM, by contrast echocardiography (preceded by anteroposterior chest radiograph) or computed tomography of the chest. Pulmonary hypertension is rare in HHT, and may be due either to systemic arteriovenous shunting in the liver increasing cardiac output or be clinically and histologically indistinguishable from idiopathic pulmonary arterial hypertension. Pulmonary hypertension is detected by systematic examination of right cardiac cavities and tricuspid regurgitation flow at echocardiography, and the diagnosis is established by right heart catheterization.
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PMID:Pulmonary vascular manifestations of hereditary hemorrhagic telangiectasia (rendu-osler disease). 1764 82

A 74-year-old man with a history of diabetes and arterial hypertension, presented with right ventricular failure, remarkable jugular venous distension, hepatomegaly, and swelling of the lower extremities. He was complaining of atypical chest pain and was referred for an echocardiogram and a myocardial perfusion SPECT imaging study. The echocardiogram showed normal left ventricular function with a dilated right atrium and right ventricle, severe tricuspid regurgitation, pulmonary hypertension, and an atrial septal defect with bidirectional shunt. The SPECT images showed normal left ventricular function with no areas of induced ischemia but an impressive right ventricle with severe dilatation and hypertrophy. A right ventricular "perfusion abnormality," consistent with ischemic changes, seen on stress but less evident on rest images was demonstrated on the dual isotope (Tl-201 rest/Tc-99m MIBI stress) protocol but not seen on the single isotope study (rest/stressTc-99m MIBI). Coronary angiogram showed diffuse coronary atherosclerosis but without significant obstruction.
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PMID:Right ventricular wall "ischemia" findings using a dual isotope protocol. 1766 45

Elevated serum brain natriuretic peptide (BNP) released from myocytes of ventricles upon stretch have been found in patients with isolated right ventricular (RV) pressure overload. However, limited data suggest that serum BNP may be elevated in systemic sclerosis (SSc) patients, especially with RV dysfunction. We assessed serum N-terminal proBNP (NT-proBNP) in SSc and evaluated whether it reflects the severity of RV overload. We prospectively studied 51 consecutive patients (47F, mean age 53.3 +/- 15.2 years) with SSc (mean disease duration 9 +/- 12.4 years). The control group formed 31 healthy subjects (27F, mean age 52.6 +/- 12.1 years). NT-proBNP level, 6-minute walking test (6MWT), and transthoracic echocardiography (TTE) for the assessment of RV overload were performed. Serum NT-proBNP exceeded the reference value of 125 pg/mL in 31 (61%) SSc patients. The mean serum log NT-proBNP concentration in SSc was higher than in controls (2.138 +/- 0.527 vs. 1.634 +/- 0.420 pg/mL, p < 0.001). 13 (25%) SSc patients have tricuspid regurgitation peak gradient (TRPG) exceeding 31 mmHg reflecting pulmonary arterial hypertension (PAH). The SSc presented other echocardiographic signs of RV overload. Mean 6MWT distance was shorter in SSc than in controls (528 +/- 100 vs. 617 +/- 80 m, p < 0.001). NT-proBNP level correlated positively with TRPG, RV diameter, RV Tei index and negatively with 6MWT distance. ROC analysis identified >115 pg/ml as the best NT-proBNP threshold predicting PAH for SSc patients (sensitivity 92%, specificity 44%). Results of our study suggest that NT-proBNP measurement is a useful screening method for PAH in SSc patients. Since elevated plasma NT-proBNP level reflects the degree of right ventricular overload and limitation of exercise capacity, abnormal NT-proBNP levels should imply further evaluation including echocardiography.
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PMID:Non-invasive diagnostic and functional evaluation of cardiac involvement in patients with systemic sclerosis. 1825 71

Aim of the study was to investigate interrelationship between serum markers of myocardial fibrosis: matrix metalloproteinase -1 (MMP-1), tissue inhibitor of metalloproteinase-1 (TIMP-1) and parameters of echocardiography in patients with arterial hypertension (AH) and paroxysmal form of atrial fibrillation (n=39). We revealed positive correlation of levels of TIMP-1 with thickness of interventricular septum in diastole (r=0,47, p=0,02), peak velocity of late filling of the right ventricle (r=0,46, p=0,01), and negative relation between MMP-1 levels and degree of mitral and tricuspid regurgitation (r=0,43, p=0,005 and r=0,38, p=0,04, respectively). In the group of patients with increased left ventricular myocardial mass index (LVMMI) TIMP-1 level was significantly higher than in patients with normal LVMMI (p < 0,05). In the group combining patients with concentric and eccentric LV hypertrophy TIMP-1 level was significantly higher than in the group combining patients with LV concentric remodeling and normal geometry (p < 0,05). No correlations were revealed between MMP-1 and TIMP-1 levels and parameters of diastolic dysfunction. In patients with AH increase of serum concentrations of TIMP-1 was associated with increased thickness of interventricular septum, increase of LVMMI, and with prognostically unfavorable types of LV remodeling.
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PMID:[Metalloproteinase activity of the blood in patients with arterial hypertension with paroxysmal form of atrial fibrillation]. 1826 Sep 72

The most recognizable features of hyperthyroidism are those that result from the effects of triiodothyronine (T3) on the heart and cardiovascular system: decreased systemic vascular resistance and increased resting heart rate, left ventricular contractility, blood volume, and cardiac output. Although these measures of cardiac performance are enhanced in hyperthyroidism, the finding of clinical cardiac failure can be somewhat paradoxical. About 6% of thyrotoxic individuals develop symptoms of heart failure, but less than 1% develop dilated -cardiomyopathy with impaired left ventricular systolic function. Heart failure resulting from thyrotoxicosis is due to a tachycardia-mediated mechanism leading to an increased level of cytosolic calcium during diastole with reduced ventricular contractility and diastolic dysfunction, often with tricuspid regurgitation. Pulmonary artery hypertension in thyrotoxicosis is gaining awareness as a cause of isolated right-sided heart failure. In both cases, older individuals are more likely to be affected. Treatment needs to be directed at management of the acute cardiovascular complications, control of the heart rate, and thyroid-specific therapy to restore a euthyroid state that will lead to resolution of the signs and symptoms of heart failure.
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PMID:Thyrotoxic cardiac disease. 1875 67

A 46-year-old woman presented with arthralgia. She had a history of fluctuating liver function impairment for 6 months. Laboratory investigations revealed elevated liver function test results, positive antinuclear antibodies and elevated serum IgG. The histological findings of a liver biopsy were interface hepatitis accompanied by plasmocytic infiltration with bridging fibrosis. There was no evidence of cirrhosis on pathological examination and no portal hypertension on endoscopic and radiographic studies. Autoimmune hepatitis was diagnosed, and treatment with prednisolone improved the liver dysfunction. After 6 months, she complained of dyspnea. Doppler echocardiography showed a dilated right ventricle, severe tricuspid insufficiency, and systolic pulmonary arterial pressure indicative of pulmonary arterial hypertension. We report this rare case of autoimmune hepatitis with pulmonary arterial hypertension.
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PMID:Autoimmune hepatitis associated with pulmonary arterial hypertension. 1901 10

The most common etiologies of myocardial infarction in the perinatal period are congenital heart disease, coronary artery lesions, thromboembolism and perinatal asphyxia. Cardiac abnormalities in perinatal asphyxia include tricuspid regurgitation and mitral regurgitation associated with transient myocardial ischemia of the newborn. Patent foramen ovale is a frequent remnant of the fetal circulation. Persistent hypoxia sometimes causes pulmonary arterial hypertension with consequent right to left shunt across patent ductus arteriosus and foramen ovale. We describe a case of tricuspid regurgitation, mitral regurgitation, and patent foramen ovale in a 15-day-old newborn male infant with a history of perinatal asphyxia. Also this case focuses attention on the perinatal asphyxia.
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PMID:Perinatal asphyxia and cardiac abnormalities. 1921 77


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