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ORIGINAL ARTICLE
Year : 2014  |  Volume : 17  |  Issue : 4  |  Page : 125-127

Comparison of echocardiographic parameters among patients with pulmonary hypertension treated with statin and those without


Department of Medicine, Division of Cardiology, University of Dammam, Dammam, Saudi Arabia

Date of Web Publication11-Dec-2014

Correspondence Address:
Mohammed Almansori
Department of Medicine, Division of Cardiology, University of Dammam, P. O. Box 12875, Dammam 31483
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1118-8561.146813

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  Abstract 

Introduction: Pulmonary hypertension is a progressive disease where endothelial dysfunction plays an important role in its etiology. Statins have been considered a therapeutic option for pulmonary hypertension due to their pleiotropic effects. Materials and Methods: We investigated the association between statin use and echocardiographic parameters in 73 patients with pulmonary hypertension (23 patients were on statin and 50 patients were not taking statin). Results: Our study showed no association between statin use and different echocardiographic parameters used to evaluation pulmonary hypertension though there was a trend toward less right ventricular dilatation favoring the statin group (25.20 ± 14.7 mm vs. 29.7 ± 9.5) with a P = 0.052. Conclusion: We observed noassociation between statin use and echocardiographic findings in patients with pulmonary hypertension. A larger scale studies are need to confirm our findings.

Keywords: Echocardiography, pulmonary hypertension, statin


How to cite this article:
Almansori M. Comparison of echocardiographic parameters among patients with pulmonary hypertension treated with statin and those without. Sahel Med J 2014;17:125-7

How to cite this URL:
Almansori M. Comparison of echocardiographic parameters among patients with pulmonary hypertension treated with statin and those without. Sahel Med J [serial online] 2014 [cited 2022 Aug 10];17:125-7. Available from: https://www.smjonline.org/text.asp?2014/17/4/125/146813


  Introduction Top


Pulmonary arterial hypertension (PAH) is a progressive disease, which has a multifactorial etiology that includes endothelial dysfunction as a key component with subsequent vasoconstriction, vascular remodeling and thrombosis. This results in progressive increase in pulmonary vascular resistance, right-sided heart failure and premature death. [1] Management strategies include oxygen, diuretics, digoxin, calcium channel antagonists, prostacyclin analogues, endothelin receptor antagonists, phosphodiesterase type 5 inhibitors and anticoagulation therapy, and lung transplantation. [1],[2] Statins have been considered a therapeutic option for patients with pulmonary hypertension. This is based on their pleiotropic effects including improved endothelial function, inhibition of vascular cell proliferation, reduction in thrombogenic response as well as attenuation of oxidative stress and inflammation. [1],[2]

In humans, there are few studies on the effect of statin in patients with PAH. [3],[4],[5],[6] Kao in 2005 [3] conducted an open-label observational study in 16 patients with PAH and noticed improvement in 6-min-walk performance, improvement in cardiac output and a decrease in right ventricular systolic pressure. Barreto et al. in 2008 [4] conducted a placebo-controlled study involving 60 patients with PAH who were randomly assigned to rosuvastatin or placebo for 6 months and observed a significant reduction in plasma level of P-selectin that is an important factor in inflammation and thrombosis. In 2009 Lee et al. [5] conducted a double-blind study involving 53 patients with chronic obstructive pulmonary disease and pulmonary hypertension that were given pravastatin or placebo for 6 months and concluded that pravastatin significantly improved functional capacity in PAH. Wilkins et al. [6] randomized 42 patients with PAH to receive simvastatin or placebo for 6 months and noticed that simvastatin, when added to conventional therapy produced a small and transient early reduction in right ventricular mass and pro-B-type natriuretic peptide level which was not sustained over a period of 12 months. The current study investigated the presence of an association between statin use and different echocardiographic parameters in patients with pulmonary hypertension.


  Materials and methods Top


This is a retrospective review involving all patients with PAH at University Hospital in Saudi Arabia from January 2002 to December 2012. Data was collected from the medical records and hospital database. Two groups of patient were identified: patients who were on statin at the time of diagnosis and those who were not on statin. The diagnosis of pulmonary hypertension was based on echocardiographically derived systolic pulmonary pressure of more than 30 mmHg as estimated from the tricuspid regurgitation velocity or an elevated mean pulmonary pressure more than 25 mmHg. [7] Patients younger than 18 years and those with significantly missing data were excluded. The echocardiogram report at the time of the diagnosis were reviewed and the following parameters were collected: diastolic mid-right ventricular diameter, tricuspid regurgitation velocity obtained with continuous wave Doppler from the right ventricular inflow or apical four-chamber view position, right ventricular systolic pressure (applying the continuity equation to tricuspid regurgitation velocity and adding the right atrial pressure which is estimated from the inspiratory collapse of the inferior vena cava), [8],[9],[10],[11] mean pulmonary artery pressure (MPAP) (estimated by right ventricular out low tract acceleration time according to Mahan's equation, MPAP = 79-0.45 [acceleration time] [12] ) and left ventricular ejection fraction. The data and baseline characteristics were computed using means and standard deviations for continuous variables and percentages for dichotomous variables. The P values for the comparison groups were calculated using t-test for continuous data and Chi-square test for the dichotomous data (Fisher's exact test was applied when cell count was small).


  Results Top


A total of 73 patients were identified to have pulmonary hypertension, 23 patients were on statin and 50 patients were not on statin at the time of the diagnosis. Most of the patients in the statin group were on atorvastatin while only 3 patients were on 20 mg of simvastatin [Figure 1]. The baseline characteristics and clinical history of the two groups are summarized in [Table 1]. Patients in the statin group were older (67.5 ± 11.3 years vs. 50 ± 17.6 years; P < 0.0001) and had higher serum creatinine level (2.5 ± 2.2 mg/dl vs. 1.4 ± 1.5 mg/dl; P = 0.016). The statin group patients had statistically higher percentage of coronary artery disease, diabetes mellitus, hypertension, dyslipidemia and history of cigarette smoking. The analysis of different echocardiographic parameters is shown in [Table 2]. Patients who were not on statin had statistically significant higher ejection fraction (63.5% ±12.2% vs. 53.7% ±14.7%; P = 0.004). We observed that the right ventricular diameter was higher among patients who were not on statin than the statin treated group though the difference was insignificant (25.2 ± 14.7 mm vs. 29.7 ± 9.5; P = 0.052). There were no significant differences between the two groups in regard to pulmonary artery diameter, tricuspid valve regurgitation velocity, right ventricular systolic pressure and pulmonary artery pressure.
Figure 1: (a) Distribution of simvastatin and atorvastatin in the statin group. (b) Distribution of different atorvastatin dosages in the statin group

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Table 1: Baseline clinical characteristics of patients


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Table 2: Echocardiographic difference between statin and non-statin group


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  Discussion Top


Previous studies looked at different clinical outcomes and chemical variables in patients with pulmonary hypertension who were given statins and suggested possible benefit of treatment with statin which is largely as a result of effect of mediators controlling vasoconstriction, vasodilation and vascular cell proliferation leading to vascular remodeling. The current study look at the association between echocardiographic variables and statin use in this group of patients. Patients in the statin group were older and had more diabetes mellitus, hypertension, dyslipidemia, coronary artery disease and smoking history. These conditions are reflective of the reasons for starting statin therapy as these patients were more susceptible to development of atherosclerosis. We observed no association between statin use and most of echocardiographic parameters used to evaluation pulmonary hypertension [Table 2]. The significant difference in ejection fraction favoring the no-statin group is obviously related to the higher prevalence of diabetes mellitus, hypertension and coronary artery disease in the statin group. It may also indicate that the pulmonary hypertension in this group is attributed to left ventricular pathology. Interestingly, our study showed marked though insignificant less right ventricular dilatation in the statin group (25.2 ± 14.7 mm vs. 29.7 ± 9.5;P = 0.052). Clinical improvement in 6-min-walk and functional capacity has been noticed in previous studies.

[Figure 1] shows that 87% of the patient in the statin group received atorvastatin and out of these, 75% received moderate-intensity statin therapy (atorvastatin 10 and 20 mg). [13] Although not tested, a high-intensity statin therapy might have an impact on patient with pulmonary hypertension.

Our study adds little to the accumulating evidence that statin may have a role in the management of patients with pulmonary hypertension. Moreover, it has certain limitations including the retrospective nature of the study, lack of catheter-derived measurement of pulmonary pressure, lack of information about the duration of statin treatment and the small sample size.


  Acknowledgments Top


We would like to express our appreciation to Dr. Hisham A. Elsayed, cardiology specialist at King Fahad Hospital of the University for his efforts with data extraction.

 
  References Top

1.
Newman JH, Fanburg BL, Archer SL, Badesch DB, Barst RJ, Garcia JG, et al. Pulmonary arterial hypertension: Future directions: Report of a National Heart, Lung and Blood Institute/Office of Rare Diseases workshop. Circulation 2004;109:2947-52.  Back to cited text no. 1
    
2.
Toshner M, Tajsic T, Morrell NW. Pulmonary hypertension: Advances in pathogenesis and treatment. Br Med Bull 2010;94:21-32.  Back to cited text no. 2
    
3.
Kao PN. Simvastatin treatment of pulmonary hypertension: An observational case series. Chest 2005;127:1446-52.  Back to cited text no. 3
    
4.
Barreto AC, Maeda NY, Soares RP, Cícero C, Lopes AA. Rosuvastatin and vascular dysfunction markers in pulmonary arterial hypertension: A placebo-controlled study. Braz J Med Biol Res 2008;41:657-63.  Back to cited text no. 4
    
5.
Lee TM, Chen CC, Shen HN, Chang NC. Effects of pravastatin on functional capacity in patients with chronic obstructive pulmonary disease and pulmonary hypertension. Clin Sci (Lond) 2009;116:497-505.  Back to cited text no. 5
    
6.
Wilkins MR, Ali O, Bradlow W, Wharton J, Taegtmeyer A, Rhodes CJ, et al. Simvastatin as a treatment for pulmonary hypertension trial. Am J Respir Crit Care Med 2010;181:1106-13.  Back to cited text no. 6
    
7.
McLaughlin VV, Archer SL, Badesch DB, Barst RJ, Farber HW, Lindner JR, et al. ACCF/AHA 2009 expert consensus document on pulmonary hypertension a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents and the American Heart Association developed in collaboration with the American College of Chest Physicians; American Thoracic Society, Inc.; and the Pulmonary Hypertension Association. J Am Coll Cardiol 2009;53:1573-619.  Back to cited text no. 7
    
8.
Hatle L, Angelsen BA, Tromsdal A. Non-invasive estimation of pulmonary artery systolic pressure with Doppler ultrasound. Br Heart J 1981;45:157-65.  Back to cited text no. 8
    
9.
Yock PG, Popp RL. Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation 1984;70:657-62.  Back to cited text no. 9
    
10.
Currie PJ, Seward JB, Chan KL, Fyfe DA, Hagler DJ, Mair DD, et al. Continuous wave Doppler determination of right ventricular pressure: A simultaneous Doppler-catheterization study in 127 patients. J Am Coll Cardiol 1985;6:750-6.  Back to cited text no. 10
    
11.
Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol 1990;66:493-6.  Back to cited text no. 11
    
12.
Mahan G, Dabestani A, Gardin J, Allfie A, Burn C, Henry W, et al. Estimation of pulmonary artery pressure by pulsed Doppler echocardiography. Circulation 1983;68 (Suppl 3) III: 367.  Back to cited text no. 12
    
13.
Stone NJ, Robinson J, Lichtenstein AH, Bairey Merz CN, Lloyd-Jones DM, Blum CB, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013; published online before print November 12 2013.  Back to cited text no. 13
    


    Figures

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    Tables

  [Table 1], [Table 2]



 

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