Determinants of right ventricular pressure in mild hypertension.

OBJECTIVE : Doppler echocardiography was used to define reference values and determinants of tricuspid regurgitation peak velocity (TRV) in hypertensive patients. A TRV value > 2.5 m/s is the threshold usually defining abnormal right ventricular systolic pressure. DESIGN AND PATIENTS : Doppler echocardiography was performed in 320 consecutive uncomplicated hypertensive patients, without overt pulmonary or heart disease. Doppler echocardiography included LV mass measurement, LV inflow and pulmonary venous flow analysis, LV systolic function and TRV measurements. RESULTS : Among 320 patients, 255 had normal TRV < 2.5 m/s and 65 had elevated TRV > or = 2.5 m/s. Compared with the normal TRV group, the elevated TRV group was older (60 versus 50 years, P < 0.0001), systolic blood pressure was higher (156 versus 151 mmHg, P = 0.02) and antihypertensive therapy was more frequent (68 versus 51%, P = 0.02); indexed LV mass was higher (45.4 versus 40.6 g/m2.7, P = 0.001), pulmonary D wave peak velocity was higher (42 versus 38 cm/s, P = 0.03). In univariate analysis, age was the most predictive variable of TRV (r = 0.36). In multivariate analysis, three variables were independently related to TRV: age, LV mass, pulmonary D wave (multiple r = 0.47). CONCLUSION : In mild hypertension, TRV is independently related to age, and to a lesser extent, to LV morphology and LV filling pressure. In clinical practice, age should be taken into account to interpret TRV.     

Accuracy of Doppler-estimated pulmonary vascular resistance in patients before liver transplantation

The hyperdynamic circulation associated with cirrhosis is typically characterized by high cardiac output and low systemic and pulmonary vascular resistance (PVR). Approximately 4% of cirrhotic patients develop portopulmonary hypertension, which is an important predictor of hemodynamic instability after orthotopic liver transplantation. Doppler estimation of pulmonary artery systolic pressure (PASP) is used as a screening test for the presence of portopulmonary hypertension. We tested the accuracy of a noninvasive measurement of PVR (ratio of peak tricuspid regurgitant velocity [TRV] to right ventricular outflow tract velocity time integral [VTI RVOT]) to detect increased PVR in a population before liver transplantation. We compared test characteristics of the TRV/VTI RVOT ratio to echocardiographically derived PASP for detection of invasively measured PVR >1.5 Wood units. There was no significant correlation between Doppler-derived PASP and invasively measured PVR. There was a moderate and significant correlation between TRV/VTI RVOT ratio and invasively measured PVR. Compared with Doppler-derived PASP, the TRV/VTI RVOT ratio was a more accurate test for PVR >1.5 Wood units. Using a cut-off value of TRV/VTI RVOT >0.12, the sensitivity and negative predictive value for PVR >1.5 Wood units were 100%. In conclusion, the TRV/VTI RVOT ratio is a more accurate screening test for the presence of portopulmonary hypertension than PASP in patients undergoing orthotopic liver transplantation. Routine use of this ratio may decrease the need for invasive hemodynamic assessment in this patient population.     

Cardiac correlates of exercise induced pulmonary hypertension in patients with chronic heart failure due to left ventricular systolic dysfunction

BACKGROUND: Patients with chronic heart failure (CHF) due to left ventricular systolic dysfunction (LVSD) may develop pulmonary hypertension at rest and during exercise. The cardiac correlates of pulmonary hypertension have been ascertained in the resting state, but seldom during exercise in these patients. AIMS: We sought to determine the cardiac correlates of exercise induced pulmonary hypertension in patients with LVSD by monitoring the estimated pulmonary artery systolic pressure (PASP) by continuous Doppler echocardiography during semirecumbent bicycle exercise. METHODS: Eighty-five patients (mean age 57 +/- 13 years, 75% male) with CHF due to LVSD (LV ejection fraction [EF] <45%, mean LVEF 26 +/- 8%) were studied. RESULTS: Mitral effective regurgitant orifice area and E-wave were independent predictors of resting PASP. Resting PASP and exercise induced changes in PASP were unrelated (r =-0.08, P = 0.45). Decrease in LV end-systolic volume, increase in left atrial (LA) area, resting LV asynchrony, and decreased tricuspid annular plane systolic excursion (TAPSE) were independent predictors of exercise PASP. CONCLUSIONS: Resting LV asynchrony, impaired LV contractile reserve, and increase in LA dilatation correlate with the severity of exercise induced pulmonary hypertension in patients with CHF due to LVSD, while right ventricular systolic dysfunction is inversely related to the severity of exercise induced pulmonary hypertension.     

Clinical and haemodynamic effects of oral metoprolol therapy in dilated cardiomyopathy

The clinical and haemodynamic effects of oral metoprolol therapy were assessed in thirty patients of dilated cardiomyopathy, aged 14-58 (33 +/- 10.9) years. After baseline haemodynamic study, metoprolol was administered in a dose of 25-100 mg/day (mean 87.0 +/- 25.1 mg/day). Before start of therapy, 13 patients were in NYHA symptom class IV, 14 were in NYHA class III and 3 were in NYHA class II. Symptomatic improvement was seen on oral metoprolol therapy in all patients except one. Six months after therapy 13 patients were asymptomatic, 16 were in NYHA class II, while 1 patient continued to be in NYHA class III. Repeat haemodynamic study in 15 patients done at a mean of 5.7 months showed a significant fall in the right ventricular end diastolic pressure (from 9.1 +/- 4.4 to 5.7 +/- 2.9 mm Hg, p less than 0.01), mean pulmonary artery pressure (from 32.3 +/- 13 to 24.5 +/- 10.3 mmHg, P less than 0.01) and mean pulmonary capillary pressure (from 23.3 +/- 10.3 mmHg to 14.7 +/- 7.4 mmHg, P less than 0.01). The left ventricular ejection fraction increased from 18.8 +/- 6.3 to 24.0 +/- 7.3 per cent, (P less than 0.05), while no significant change was observed in the cardiac index (2.43 +/- 0.47 to 2.66 +/- 0.83 L/min/m2, p = NS). These data suggest improvement in diastolic and systolic left ventricular function after metoprolol therapy.     

Oral sildenafil improves primary pulmonary hypertension refractory to epoprostenol.

BACKGROUND: Epoprostenol (prostaglandin I(2)) has become recognized as a therapeutic breakthrough that can improve hemodynamics and survival in patients with primary pulmonary hypertension (PPH). However, a significant number of patients have PPH that is refractory to epoprostenol, and lung transplantation has been the only remaining treatment option. METHODS AND RESULTS: The study subjects included 20 consecutive patients with PPH (mean pulmonary arterial pressure: 65+/-15 mmHg) who had received epoprostenol for more than 12 months. The patients were divided into 2 groups; responders and non-responders. In the non-responders, New York Heart Association (NYHA) functional class did not improve and mean right atrial pressure (mRA) increased to 8 mmHg or more, and additional sildenafil, a phosphodiesterase-5 inhibitor, was started. Six patients were included in the non-responders, whose mRA was 9+/-5 mmHg before and significantly increased to 13+/-3 mmHg after epoprostenol administration (p < 0.05). One patient died and the other 5 patients received oral sildenafil. The mRA of 12+/-4 mmHg (value before sildenafil) improved to 8+/-5 mmHg after sildenafil administration. Three patients were classified in the NYHA functional class 4 and improved to class 3, and 2 patients were in class 3 and remained in the same class after the addition of sildenafil. CONCLUSIONS: In patients with severe PPH refractory to epoprostenol treatment, additional oral sildenafil can improve pulmonary hemodynamics and symptoms. The combination therapy of epoprostenol and sildenafil is a new medical treatment to attempt before progressing to lung transplantation for patients with PPH refractory to epoprostenol.     

Early reversal of right ventricular dysfunction in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator

To assess abnormalities of right heart function and their reversal with thrombolysis in pulmonary embolism, serial imaging and Doppler echocardiographic studies were performed before and after a 6 hour intravenous infusion of 80 to 90 mg of recombinant tissue-type plasminogen activator (rt-PA) in seven patients with segmental or lobar acute pulmonary embolism. None of the five men and two women had known prior pulmonary hypertension. Substantial clot lysis and improvement in pulmonary blood flow, as determined by serial pulmonary angiography and perfusion lung scanning, were achieved in all. Coincident with clot lysis, pulmonary artery systolic pressure decreased (from 42 +/- 11 to 26 +/- 7 mm Hg, p less than 0.005), right ventricular diameter decreased (from 3.9 +/- 1.0 to 2.0 +/- 0.5 cm, p less than 0.005) and left ventricular diameter increased (from 3.7 +/- 0.9 to 4.4 +/- 0.6 cm, p less than 0.01). Right ventricular wall movement, initially mildly, moderately or severely hypokinetic in one, two and four patients, respectively, normalized in five and improved to mild hypokinesia in two. Tricuspid regurgitation was present before lytic therapy in six patients. In five, flow velocity in the tricuspid regurgitant jets indicated a peak systolic right ventricular minus right atrial pressure gradient of 25 to 52 mm Hg. Tricuspid regurgitation was detected early after lytic therapy in only two patients. Systolic septal flattening was noted before but not after lysis. These findings confirm that pulmonary emboli may result in appreciable right ventricular dysfunction and dilation, resultant tricuspid regurgitation, abnormal septal position and decreased left ventricular size.(ABSTRACT TRUNCATED AT 250 WORDS)     

Incorporation of pulmonary vascular resistance measurement into standard echocardiography: implications for assessment of pulmonary hypertension

Doppler estimation of pulmonary artery systolic pressure (PASP) from tricuspid regurgitation velocity is a simple approach to the detection of pulmonary hypertension but may be influenced by right ventricular stroke volume. We sought the clinical utility of incorporating Doppler calculation of pulmonary vascular resistance (PVR) into determination of pulmonary hypertension in 578 consecutive patients with tricuspid regurgitation. Right atrial pressure was estimated from vena caval dimensions and collapsibility. Pulmonary hypertension was classified on the basis of a) PASP >35 mmHg, b) age-/gender normalized PASP, c) PVR >2 Wood units. The mean PASP was 40 +/- 13 mmHg and PVR was 1.9 +/- 0.8 Wood units. Standard PASP identified pulmonary hypertension in 58%, compared with 36% by age-/gender normalized PASP (P < 0.0001), and 31% by PVR (P < 0.0001). Of patients who had pulmonary hypertension by PASP, 33% were reclassified as normal on the basis of PVR and 6% were reclassified from normal to pulmonary hypertension. PVR is easy to incorporate into a standard echo exam, and identifies a small group with normal PASP as having PAH, and a larger group of apparently increased PASP as normal.     

Echo Doppler predictors of pulmonary artery hypertension in patients with systemic sclerosis

Objectives: Evaluate echocardiographic predictors of pulmonary artery hypertension (PAH) in a prospective cohort of patients with systemic sclerosis (SSc). Methods: 38 patients with SSc who did not have PAH and significant left heart disease, with peak tricuspid regurgitant velocity (TRV) ≤ 2.8 m/sec and systolic pulmonary artery pressure (sPAP) < 40 mmHg on echo Doppler were enrolled. Patients underwent: clinical assessment, NT‐proBNP, and DLco measurements. Echo Doppler evaluation included right ventricular (RV) dimensions, tricuspid annular plan systolic excursion, fractional area change, tricuspid DTI systolic velocity, Tei index, pulmonary flow acceleration time (AcT), ratio of TRV to RV outflow tract time–velocity integral (TVI) and a parameter of disturbed RV ejection (TRV/AcT). After a planned 12‐month follow‐up we evaluated the predictive value of these parameters for the development of PAH, as demonstrated by right heart catheterization (RHC). Criteria for RHC were TRV ≥ 3 m/sec or sPAP ≥ 40 mmHg. Results: Four patients developed PAH. Only TRV/TVI and TRV/AcT ratios significantly predicted PAH development (TRV/TVI ratio ≥ 0.16 [predefined and ROC confirmed]: OR 99, CI 95%: 4.865–2015, P = 0.004; TRV/AcT ratio ≥ 0.022 [predefined and ROC confirmed]: OR 12.68, CI 95% 1.163–379.3, P = 0.036). Both parameters showed a good diagnostic power (TRV/TVI ratio: ROC area 79%, sensitivity 75%, specificity 97% and diagnostic accuracy 94.74% for cutoff value of 0.16; TRV/AcT ratio: ROC area 75%, sensitivity 75%, specificity 71% and diagnostic accuracy 72% for cutoff value of 0.022). Conclusions: This prospective study identified increased values of the two ratios TRV/TVI and TRV/AcT as predictors of PAH in SSc. (Echocardiography 2011;28:860‐869)     

Functional tricuspid regurgitation following replacement of the mitral valve.

In this series, the effect of replacement of the mitral valve was examined in 86/900 (9.6%) patients who had developed moderate functional tricuspid regurgitation, secondary to rheumatic mitral valvar disease. These patients were subdivided according to the severity of pulmonary hypertension and impairment of right ventricular function. Forty-six patients presented with severe pulmonary hypertension and 40 patients had moderate pulmonary hypertension (mean main pulmonary arterial pressure: 78 +/- 14 mmHg vs 41 +/- 6 mmHg; P less than 0.05). The latter had more advanced disease, greater impairment of right ventricular function and dilatation of the right heart chambers. Functional tricuspid regurgitation regressed in 38/42 survivors with severe pulmonary hypertension and persisted or progressed significantly in 22/34 survivors with impaired right ventricular function despite successful replacement of the mitral valve. The latter underwent replacement of the tricuspid valve (n = 16) or tricuspid annuloplasty (n = 6), at a mean interval of 44 +/- 4.4 months after replacement of the mitral valve, which resulted in 8/22 (23.5%) early deaths. Functional tricuspid regurgitation is more likely to persist in patients with advanced right ventricular failure. Tricuspid valvar competence should be restored in these patients at initial replacement of the mitral valve.     

Epoprostenol in chronic thromboembolic pulmonary hypertension with distal lesions.

BACKGROUND: Although patients with primary pulmonary hypertension and patients with chronic thromboembolic pulmonary hypertension with distal lesions may share similar pathophysiological characteristics, scarce information is available on the usefulness of epoprostenol in this form of secondary pulmonary hypertension. The aim of this study was to evaluate the feasibility, safety and efficacy of epoprostenol therapy in surgically untreatable patients with chronic thromboembolic pulmonary hypertension. METHODS: Continuous infusive therapy with epoprostenol was undertaken in 16 patients with primary pulmonary hypertension and in 11 surgically untreatable thromboembolic pulmonary hypertension patients. The median follow-up was 12.4 months (range 6-23 months). Patients underwent clinical, echocardiographic and hemodynamic evaluation at baseline and a 6-min walk test every 3 months after beginning epoprostenol; ultrasound evaluations were repeated in a subgroup of patients. RESULTS: Epoprostenol therapy improved the clinical status, exercise tolerance and NYHA functional class. A greater left ventricular end-diastolic volume was recorded at echocardiography in both groups. CONCLUSIONS: Epoprostenol therapy may be feasible, safe and clinically effective in patients with surgically untreatable chronic thromboembolic pulmonary hypertension.     

Effect of tricuspid annuloplasty in mitral/aortic valve replacement on the clinical aspects and global function of the right heart chamber

The clinical improvement after mitral or aortic valve surgery is primarily due to the correction of the aortic/mitral valve function and the subsequent decrease of pulmonary artery pressure. The hemodynamic effect of an additional tricuspid annuloplasty, however, is still unclear. To assess the influence of a tricuspid annuloplasty using DeVega- or Carpentier-technique on the clinical outcome, hemodynamics, and right ventricular function in patients with moderate to severe tricuspid insufficiency, 38 patients were studied pre- and 11 +/- 4 months postoperatively. The clinical degree of left heart failure was graded according to the criteria of the NYHA. The extent of right heart failure (RHF) was determined using a clinical score from 0 (no signs) to 3 (severe RHF with pleural effusion/ascites). Mean pulmonary artery pressure (PAPm), end-diastolic volume index (RVEDVI), and ejection fraction (RVEF) of the right ventricle using biplane cineventriculography, as well as the angiographic and dopplerechocardiographic degree of tricuspid insufficiency were determined. The patients were assigned to three groups: gr.I (n = 12): preoperatively no tricuspid insufficiency (TI), gr. II (n = 12): with preop. TI and without tricuspid annuloplasty (TA), gr. III (n = 14): with preop. TI and TA. The patients of all three groups improved postoperatively from NYHA functional class III to class II (p less than 0.001). The clinical score of RHF decreased from 0.8 +/- 0.5 to 0.3 +/- 0.5 in gr. I, from 1.4 +/- 1.1 to 0.6 +/- 0.7 in gr. II, and from 1.7 +/- 1.0 to 0.8 +/- 0.8 in gr. III (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Epoprostenol for treatment of pulmonary hypertension in patients with systemic lupus erythematosus

OBJECTIVE: Pulmonary hypertension with pathological changes similar to those observed in primary pulmonary hypertension occurs in patients with systemic lupus erythematosus (SLE). The efficacy of chronic epoprostenol therapy in SLE has not been well described. The objective of this paper is to describe our experience with long-term epoprostenol therapy in patients with pulmonary hypertension associated with SLE. DESIGN: Case series of six patients with SLE and associated pulmonary hypertension receiving chronic treatment with epoprostenol. RESULTS: All 6 patients had severe pulmonary hypertension. Mean pulmonary artery pressure (mPAP) was 57 +/- 9 mm Hg (mean +/- SD), and pulmonary vascular resistance was 14 +/- 7 units before beginning therapy with epoprostenol. In 4 patients who underwent repeat hemodynamic evaluation (9 to 16 months after starting epoprostenol), mean pulmonary artery pressure decreased by 38 +/- 21% and pulmonary vascular resistance by 58 +/- 12%. Clinically, all patients improved from New York Heart Association class III or IV to class I or II. Doses of epoprostenol ranged from 4 to 46 ng/kg/min, and the longest duration of therapy has been 2.5 years. Side effects from epoprostenol have not differed from those seen in patients with primary pulmonary hypertension, and except for one patient, there has been no exacerbation of SLE. CONCLUSION: Epoprostenol was effective for the treatment of pulmonary hypertension in this small group of patients with SLE. Further evaluation of epoprostenol therapy for patients with SLE and other diseases associated with pulmonary hypertension is warranted.     

Effects of epoprostenol on right ventricular hypertrophy and dilatation in pulmonary hypertension

OBJECTIVES: To gain more knowledge of changes in main pulmonary artery flow and right ventricular mass and volumes in patients with pulmonary hypertension during epoprostenol therapy. METHODS: Eleven patients (9 women) were evaluated before the start of therapy and every 4 months thereafter. Right and left ventricular volumes and masses were measured by cine MRI. Flow was measured with MRI velocity quantification. At the same times, 6-min walking tests were performed. Right-heart catheterizations were performed at baseline and after 1 year. RESULTS: Right ventricular mass in the patient group was significantly higher from that in a control group of healthy volunteers (95 +/- 26 g vs 42 +/- 10 g, p < 0.05 [mean +/- SD]), whereas the stroke volume was lower (34 +/- 11 mL vs 81 +/- 11 mL, p < 0.05). The greatest improvement in right ventricular stroke volume (to 41 +/- 11 mL, p < 0.05) took place in the first 4 months. During the 1-year follow-up, right ventricular end-diastolic volume and mass did not change, and mean pulmonary artery pressure remained nearly stable at 55 mm Hg at baseline and 53 mm Hg after 1 year. Pulmonary vascular resistance decreased by 12.5% (p = 0.06). CONCLUSIONS: From these data we conclude that epoprostenol lowers pulmonary vascular resistance, leading to an increase in pulmonary artery flow. This increase in pulmonary artery flow corresponds well with the increase in 6-min walking distance and can be noninvasively monitored by MRI (flow quantification). Right ventricular dilatation and hypertrophy are not reversed by epoprostenol therapy, but do not progress either.     

Determination of the size of the right atrium in patients with pulmonary hypertension using 2-dimensional echocardiography

Normal values for right atrial area and tricuspid annular diameter and their percentage shortening measured from the two-dimensional echocardiographic four-chamber view are now available. In this study right atrial size of patients with pulmonary hypertension is evaluated and the results compared with the M-mode findings of the right ventricle in order to detect pulmonary hypertension. Hemodynamics and echocardiograms of 60 patients (mean age 57 +/- 10 years) with mitral stenosis III-IV NYHA and concomitant pulmonary hypertension were examined. 20 patients in group I with atrial fibrillation had additional functional tricuspid incompetence. Unlike the 20 patients in group II, who had atrial fibrillation, the remaining 20 in group III were still in sinus rhythm. The mean pulmonary artery pressure was 44.1 +/- 9.3 mmHg in group I, in group II 33.9 +/- 6.3 mmHg (grp. I vs. grp. II p less than 0.001) and in group III 33.2 +/- 7.1 mmHg (grp. II vs. grp. III ns). The end-systolic index of the right atrial area in group I was 19.6 +/- 5.7 cm2/m2 and thus significantly greater than in group II with 10.6 +/- 2.3 cm2/m2 (p less than 0.001) and in group III with 9.1 +/- 2.5 cm2/m2 (p less than 0.001). The maximal diameter of the tricuspid annulus measured 24.6 +/- 5.5 mm/m2 in group I, 18.9 +/- 3.5 mm/m2 in group II (grp. I vs. grp. II p less than 0.001) and 20.2 +/- 2.2 mm/m2 in group II (grp. I vs. grp. II p less than 0.001) and 20.2 +/- 2.2 mm/m2 in group III.(ABSTRACT TRUNCATED AT 250 WORDS)     

Short-term and long-term epoprostenol (prostacyclin) therapy in pulmonary hypertension secondary to connective tissue diseases: results of a pilot study.

Continuous intravenous epoprostenol improves exercise capacity, haemodynamics, and survival in severe primary pulmonary hypertension. Pulmonary hypertension can also be life-threatening in patients with connective tissue diseases. In a prospective open monocentre uncontrolled study, the effects of epoprostenol were evaluated in patients with severe pulmonary hypertension secondary to connective tissue diseases who were unresponsive to oral vasodilators (including calcium channel blockers) and continued to be in the New York Heart Association (NYHA) functional class III or IV despite conventional medical therapy. Seventeen patients received epoprostenol administered by a portable infusion pump associated with conventional therapy (oral anticoagulants, diuretics, supplemental oxygen). During the first six weeks of therapy, two (12%) patients died, of pulmonary oedema (n = 1) and severe sepsis (n = 1). In the fifteen remaining subjects, clinical and haemodynamic parameters improved significantly at six weeks. These patients were subsequently monitored for 80+/-48 (range 14-154) weeks after initiation of epoprostenol. Five (33%) patients died, of right heart failure (n = 2), severe sepsis (n = 2) or syncope (n = 1) and two patients were successfully transplanted 24 and 52 weeks after initiation of epoprostenol. Seven of the remaining eight patients had a persistent clinical improvement. Short-term epoprostenol therapy is effective in some patients with connective tissue diseases as demonstrated by better clinical status and haemodynamics at six weeks. However, this study reports several cases of early and late major complications including severe sepsis and pulmonary oedema. Additional information is needed to evaluate the benefit: risk ratio of long-term epoprostenol therapy in pulmonary hypertension secondary to connective tissue diseases.     

Continuous intravenous epoprostenol for pulmonary hypertension due to the scleroderma spectrum of disease. A randomized, controlled trial

BACKGROUND: Pulmonary hypertension is a progressive and often fatal complication of the scleroderma spectrum of disease for which no treatment has been proven effective in a randomized trial. OBJECTIVE: To determine the effect of epoprostenol on pulmonary hypertension secondary to the scleroderma spectrum of disease. DESIGN: Randomized, open-label, controlled trial. SETTING: 17 pulmonary hypertension referral centers. PATIENTS: 111 patients with moderate to severe pulmonary hypertension. INTERVENTION: Epoprostenol plus conventional therapy or conventional therapy alone. MEASUREMENTS: The primary outcome measure was exercise capacity. Other measures were cardiopulmonary hemodynamics, signs and symptoms of pulmonary hypertension and scleroderma, and survival. RESULTS: Exercise capacity improved with epoprostenol (median distance walked in 6 minutes, 316 m at 12 weeks compared with 270 m at baseline) but decreased with conventional therapy (192 m at 12 weeks compared with 240 m at baseline). The difference between treatment groups in the median distance walked at week 12 was 108 m (95% CI, 55.2 m to 180.0 m) (P < 0.001). Hemodynamics improved at 12 weeks with epoprostenol. The changes in mean pulmonary artery pressure for the epoprostenol and conventional therapy groups were -5.0 and 0.9 mm Hg, respectively (difference, -6.0 mm Hg [CI, -9.0 to -3.0 mm Hg), and the mean changes in pulmonary vascular resistance were -4.6 and 0.9 mm Hg/L per minute, respectively (difference, -5.5 mm Hg/L per minute [CI, -7.3 to -3.7 mm Hg/L per minute). Twenty-one patients treated with epoprostenol and no patients receiving conventional therapy showed improved New York Heart Association functional class. Borg Dyspnea Scores and Dyspnea-Fatigue Ratings improved in the epoprostenol group. Trends toward greater improvement in severity of the Raynaud phenomenon and fewer new digital ulcers were seen in the epoprostenol group. Four patients in the epoprostenol group and five in the conventional therapy group died (P value not significant). Side effects of epoprostenol therapy included jaw pain, nausea, and anorexia. Adverse events related to the epoprostenol delivery system included sepsis, cellulitis, hemorrhage, and pneumothorax (4% incidence for each condition). CONCLUSIONS: Continuous epoprostenol therapy improves exercise capacity and cardiopulmonary hemodynamics in patients with pulmonary hypertension due to the scleroderma spectrum of disease.     

Oral metoprolol therapy in dilated cardiomyopathy: hemodynamic evidence for improved diastolic function accompanying amelioration of symptoms

Twenty patients with dilated cardiomyopathy (11 males and 9 females) aged from 14 to 54 (37.3 +/- 10.5) years were treated orally with metoprolol (dose 37.5 mg-100 mg/day, mean 91 +/- 18.6 mg/day) after a baseline hemodynamic study. On follow-up, all patients showed improvement in symptomatic status by at least one NYHA class within 2 to 4 weeks of the initiation of therapy. Repeat right heart study and left ventricular angiography (venous digital subtraction angiography) afer 3 to 6 months of treatment in 10 patients showed a fall in the mean pulmonary arterial wedge pressure from 24.4 +/- 9.6 to 12.8 +/- 7.7 mm Hg (P = 0.025), right ventricular end-diastolic pressure from 8.8 +/- 4.7 mm Hg to 4.5 +/- 1.9 mm Hg (P = 0.025) and mean pulmonary arterial pressure from 34.2 +/- 12.4 mm Hg to 25.9 +/- 10.9 mm Hg (P less than 0.01). There was no significant change in the left ventricular ejection fraction (18.7 +/- 1.6% vs. 22 +/- 0.48%, P = NS) or cardiac index (2.2 +/- 0.48 l/m/m2 to 2.12 +/- 0.68 l/m/m2, P = NS). These hemodynamic results indicate that the improvement in symptoms and congestive cardiac failure produced by treatment with metoprolol in patients having dilated cardiomyopathy is related to improvement in diastolic function of the myocardium.     

Abnormal right ventricular myocardial strain generation in mild pulmonary hypertension

BACKGROUND: Although right ventricular (RV) dyssynchrony has been identified in patients with severe pulmonary hypertension due to significant RV enlargement and compromise in systolic function, a more clinically relevant question pertains to RV mechanical properties in patients with mild elevation in pulmonary artery systolic pressures (PASP). METHODS: Several echocardiographic parameters and peak longitudinal strain were measured in 40 patients and divided into two groups of 20 patients based on their PASP. RESULTS: Group I included 20 individuals (mean age 48 +/- 16 years with a mean PASP of 27 +/- 5 mmHg) and Group II included 20 patients (mean age 63 +/- 14 years with a mean PASP of 49 +/- 7 mmHg.) All time intervals were adjusted for heart rate. RV fractional area change and tricuspid annular plane systolic excursion for Group I (62 +/- 12% and 2.74 +/- 0.56 cm) and Group II (49 +/- 14%; P < 0.02 and 2.09 +/- 0.40; P < 0.002) were both normal. However, Group II had lower peak longitudinal RV free wall (RVF) strain (-27.3 +/- 7.1 % vs. -31.9 +/- 8.7%, P < 0.04), longer time to peak RVF strain (448 +/- 57 ms vs. 411 +/- 43 ms; P < 0.03) and evidence of significant RV dyssynchrony (-83 +/- 55 ms vs. 1 +/- 17 ms, P < 0.00001) in contrast to Group I. CONCLUSION: In conclusion, mild elevations in PASP affect the mechanical properties of the RV and result in RV dyssynchrony despite absence of gross abnormalities in RV size or function.     

The characteristics of right ventricular function in patients with essential hypertension

Two-dimensional and pulsed Doppler echocardiography were used to evaluate the function of right ventricule in 166 patients with essential hypertension and the results were compared with those of 79 normal subjects. The pulmonary artery peak flow velocity in 100 patients without left ventricular hypertrophy (LVH) had no significant difference with that of normal controls (0.65 +/- 0.17 vs 0.63 +/- 0.18, P greater than 0.05). The tricuspid early peak flow velocity (E) decreased (0.43 +/- 0.08 vs 0.46 +/- 0.12, P less than 0.01) but the late peak flow velocity (A) increased (0.30 +/- 0.09 vs 0.24 +/- 0.06, P less than 0.001). E/A reduced also (1.57 +/- 0.53 vs 2.02 +/- 0.78, P less than 0.01). The pulmonary peak flow velocity in 66 patients with LVH elevated markedly as compared with those without LVH (0.71 +/- 0.18 vs 0.65 +/- 0.17, P less than 0.001), A increased (0.34 +/- 00.10 vs 0.30 +/- 0.09, P less than 0.001) and E/A decreased (1.29 +/- 0.37 vs 1.57 +/- 0.53, P less than 0.001). The decrement of E/A correlated with the thickness of interventricular septum and the left ventricular mass (r = -0.68 and -0.60 respectively, P less than 0.01). The results show that the diastolic function of right ventricule was damaged in the early stage of essential hypertension but the systolic function remains unchanged. The diastolic function decreased and the systolic function increased further concomitantly with the development of LVH.     

Tei指数对系统性硬皮病患者右室功能的诊断价值评估

目的应用脉冲多普勒超声(PW)测定右室Tei指数评价系统性硬皮病(SSc)患者的右室功能,并观察肺动脉高压(PH)对右室Tei指数的影响。方法纳入2009年1月~2010年1月包头医学院第一附属医院SSc患者30例作为观察组,同期纳入正常体检者30例作为对照组,应用PW对所有入组人员进行右室Tei指数测定,即测量三尖瓣口血流频谱A波终末至下一个三尖瓣口血流频谱E波起始的时间(a)和肺动脉血流频谱的起止时间(b),Tei指数=(a-b)/b;应用三尖瓣返流法估测肺动脉收缩压(PASP),并应用Pearson相关分析评价右室Tei指数和PASP的相关性。结果①病例组右室Tei指数显著高于对照组[(0.36±0.13)vs.(0.23±0.08),P0.05];②右室Tei指数与肺动脉收缩压(PASP)呈正相关(r=0.702,P0.001)。结论 SSc患者右室Tei指数显著升高,可作为提示肺动脉高压的重要指标。