Statin Therapy Decreases Myocardial Function as Evaluated Via Strain Imaging

Rubinstein, Jack; Aloka, Feras; Abela, George S.

doi:10.1002/clc.20644

Cited by 9 publications

(6 citation statements)

References 33 publications

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“…The presence of metabolic syndrome [ 24 ], a primary focus of the two aforementioned studies in which statin therapy blunted adaptations, may have limited adaptations. In addition, reduced cardiac strain with statin use may be a contributing factor [ 25 ]. It is also worthwhile to consider the trends in the post-intervention data of the current study that reflect lower muscle oxidative capacity in the presence of chronic statin therapy despite the similar relative improvement ( Fig.…”

Section: Discussionmentioning

confidence: 99%

The impact of statin therapy and aerobic exercise training on skeletal muscle and whole-body aerobic capacity

Slade

Abela

Rozman

et al. 2021

American Heart Journal Plus: Cardiology Research and Practice

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Background: Statin use is widely recognized for improving cardiovascular health, but questions remain on how statin use influences skeletal muscle, particularly mitochondrial function. Study objective, design and participants: The influence of statin therapy and exercise (EX) on aerobic capacity was determined. In Study1, skeletal muscle aerobic capacity was measured before and after 80 mg atorvastatin therapy. In Study2, aerobic capacity (skeletal muscle and whole body) was measured before and after a 12-week exercise randomized control trial in older adults (age = 67 ± 5 yrs.), a subset of which were on chronic low-moderate intensity statin therapy. Main outcome measures: Muscle oxidative capacity was determined from the phosphocreatine recovery rate constant ( k PCr) using 31 P Magnetic Resonance Spectroscopy. Whole body peak oxygen uptake (VO 2 peak) was measured during a graded exercise test with indirect calorimetry. Results: High dose statin therapy resulted in a 12% reduction in muscle oxidative capacity (pre = 1.34 ± 0.34 min −1 , post = 1.17 ± 0.25 min −1 , p = 0.004). Similarly, chronic low-moderate dose statin therapy was associated with lower muscle oxidative capacity at baseline (1.50 ± 0.35 min −1 ) compared to non-statin users (1.88 ± 0.047 min −1 , p = 0.019). Following EX, muscle oxidative capacity increased by 35–40% (statin: Pre: 1.39 ± 0.44 vs. Post: 1.88 ± 0.47 min −1 , no statin Pre: 1.86 ± 0.58 vs. Post: 2.58 ± 0.85 min −1 ) compared to control groups (Pre: 1.74 ± 0.27 vs Post: 1.75 ± 0.49 min −1 , p = 0.001). VO 2 peak increased by 11% for EX groups (Pre: 18.8 ± 2.8 vs. Post: 20.8 ± 3.0 ml·kg −1 ·min −1 ) following training compared to a small decline in controls (Pre: 21.8 ± 3.7 vs. Post: 20.8 ± 3.04 ml·kg −1 ·min −1 , p = 0.001). Conclusions: Statin therapy resulted in reduced muscle oxidative capacity. Aerobic exercise improved skeletal muscle oxidative capacity and whole-body aerobic capacity during statin therapy.

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Section: Discussionmentioning

confidence: 99%

The impact of statin therapy and aerobic exercise training on skeletal muscle and whole-body aerobic capacity

Slade

Abela

Rozman

et al. 2021

American Heart Journal Plus: Cardiology Research and Practice

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“…Rubinstein et al . [ 23 ] showed that statin therapy in hypercholesterolemic patients for at least 6 months resulted in a small decrease in myocardial function of lateral wall (measured by TDI), which could be possibly due to statin-induced myopathy of cardiac muscle. However, another study demonstrated a significant improvement in LV systolic and diastolic velocities after 6 months of atorvastatin therapy with no such change in LVEF.…”

Section: Discussionmentioning

confidence: 99%

A prospective, randomized study: Evaluation of the effect of rosuvastatin in patients with chronic obstructive pulmonary disease and pulmonary hypertension

et al. 2016

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Objectives:Statins by their anti-inflammatory and endothelial stabilizing effect can be beneficial in patients with chronic obstructive pulmonary disease (COPD) and pulmonary hypertension (PH). The present study was done to evaluate the effect of rosuvastatin on pulmonary functions and quality of life (QOL) in patients with concomitant COPD and PH.Materials and Methods:It was a prospective, randomized, double-blind, placebo-controlled, study conducted in patients with COPD and PH. A total of sixty patients were assigned to receive either rosuvastatin 10 mg or placebo once a day in addition to their conventional treatment for 12 weeks. Routine blood investigations, pulmonary functions, echocardiogram, exercise capacity, and QOL using a questionnaire were assessed at the baseline and after 12 weeks.Results:In patients of rosuvastatin group, there was a statistically significant increase in peak expiratory flow rate (PEFR) (P = 0.04) but no significant change in other pulmonary functions: Forced vital capacity (FVC), forced expiratory volume at 1 s (FVC, FEV1, FEV1/FVC), and echocardiogram parameters. There was a significant increase in 6-min walk test (6-min walk distance) (P = 0.03) at the end of 12 weeks. On comparing with placebo, rosuvastatin showed a significant reduction (P = 0.045) in COPD exacerbations while adverse effects did not differ.Conclusion:Statins have a favorable effect on patients with COPD and PH regarding the improvement in PEFR, COPD exacerbations, and exercise capacity. Such effects can be beneficial in these patients and more so in patients with concomitant coronary artery disease or hyperlipidemia where long-term benefits of statins have been established.

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“…However, these were in hypercholesterolaemic patients, so it is impossible to differentiate between improvement of serum cholesterol and direct effects on the myocardium. Interestingly, a recent study has shown that in normocholesterolaemic subjects, statin treatment improves myocardial function indexed by strain imaging [55] .…”

Section: Discussionmentioning

confidence: 99%

Caveolin Contributes to the Modulation of Basal and β-Adrenoceptor Stimulated Function of the Adult Rat Ventricular Myocyte by Simvastatin: A Novel Pleiotropic Effect

et al. 2014

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The number of people taking statins is increasing across the globe, highlighting the importance of fully understanding statins' effects on the cardiovascular system. The beneficial impact of statins extends well beyond regression of atherosclerosis to include direct effects on tissues of the cardiovascular system (‘pleiotropic effects’). Pleiotropic effects on the cardiac myocyte are often overlooked. Here we consider the contribution of the caveolin protein, whose expression and cellular distribution is dependent on cholesterol, to statin effects on the cardiac myocyte. Caveolin is a structural and regulatory component of caveolae, and is a key regulator of cardiac contractile function and adrenergic responsiveness. We employed an experimental model in which inhibition of myocyte HMG CoA reductase could be studied in the absence of paracrine influences from non-myocyte cells. Adult rat ventricular myocytes were treated with 10 µM simvastatin for 2 days. Simvastatin treatment reduced myocyte cholesterol, caveolin 3 and caveolar density. Negative inotropic and positive lusitropic effects (with corresponding changes in [Ca2+]i) were seen in statin-treated cells. Simvastatin significantly potentiated the inotropic response to β2-, but not β1-, adrenoceptor stimulation. Under conditions of β2-adrenoceptor stimulation, phosphorylation of phospholamban at Ser16 and troponin I at Ser23/24 was enhanced with statin treatment. Simvastatin increased NO production without significant effects on eNOS expression or phosphorylation (Ser1177), consistent with the reduced expression of caveolin 3, its constitutive inhibitor. In conclusion, statin treatment can reduce caveolin 3 expression, with functional consequences consistent with the known role of caveolae in the cardiac cell. These data are likely to be of significance, particularly during the early phases of statin treatment, and in patients with heart failure who have altered β-adrenoceptor signalling. In addition, as caveolin is ubiquitously expressed and has myriad tissue-specific functions, the impact of statin-dependent changes in caveolin is likely to have many other functional sequelae.

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Statin Therapy Decreases Myocardial Function as Evaluated Via Strain Imaging

Cited by 9 publications

References 33 publications

The impact of statin therapy and aerobic exercise training on skeletal muscle and whole-body aerobic capacity

The impact of statin therapy and aerobic exercise training on skeletal muscle and whole-body aerobic capacity

A prospective, randomized study: Evaluation of the effect of rosuvastatin in patients with chronic obstructive pulmonary disease and pulmonary hypertension

Caveolin Contributes to the Modulation of Basal and β-Adrenoceptor Stimulated Function of the Adult Rat Ventricular Myocyte by Simvastatin: A Novel Pleiotropic Effect

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