Skip to main content
main-content

Tipp

Weitere Artikel dieser Ausgabe durch Wischen aufrufen

Erschienen in: Wiener klinische Wochenschrift 17-18/2021

29.03.2021 | review article

The advantages of drug treatment with statins in patients with SARS-CoV-2 infection

verfasst von: Francesco Ferrara, Antonio Vitiello

Erschienen in: Wiener klinische Wochenschrift | Ausgabe 17-18/2021

Einloggen, um Zugang zu erhalten
share
TEILEN

Summary

On 11 March 2020 the World Health Organization (WHO) declared a status of global pandemic caused by the new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease 2019, COVID-19). The pandemic is currently underway, and to date has caused approximately 2.42 million deaths worldwide. The first vaccines have recently been licensed; however, research continues to identify therapeutic agents to prevent serious complications, such as anti-inflammatory, immunomodulatory, anticoagulant or antiviral agents authorized for other therapeutic indications. Epidemiological evidence shows that advanced age and comorbidities, such as diabetes, heart disease, and dyslipidemia may represent COVID-19 risk factors. In particular, in patients with hypercholesterolemia treated with statins, it is recommended that treatment should not be discontinued if COVID-19 infection occurs. The pleiotropic effects of statins are well known. In this brief review, we propose that the use of statins can potentially protect against SARS-CoV-2-induced tissue damage and improve lung function in COVID-19 patients through several pleiotropic effects. Pleiotropic effects of statins that may be a significant benefit in patients with hypercholesterolemia treated with statins and COVID-19 positive. Recent evidence shows promising results.
Literatur
4.
Zurück zum Zitat Li Q, Guan X, Wu P, et al. Early transmission dynamics in Wuhan, China, of novel Coronavirus-infected pneumonia. N Engl J Med. 2020;382:1199. PubMedPubMedCentralCrossRef Li Q, Guan X, Wu P, et al. Early transmission dynamics in Wuhan, China, of novel Coronavirus-infected pneumonia. N Engl J Med. 2020;382:1199. PubMedPubMedCentralCrossRef
6.
Zurück zum Zitat Chen N, Zhou M, et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet. 2020;395(10223):507–13. PubMedPubMedCentralCrossRef Chen N, Zhou M, et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet. 2020;395(10223):507–13. PubMedPubMedCentralCrossRef
12.
Zurück zum Zitat Guan WJ, Ni ZY, Hu Y, et al. Clinical characteristics of Coronavirus disease 2019 in China. N Engl J Med. 2020;382:1708. PubMedCrossRef Guan WJ, Ni ZY, Hu Y, et al. Clinical characteristics of Coronavirus disease 2019 in China. N Engl J Med. 2020;382:1708. PubMedCrossRef
14.
Zurück zum Zitat Chung TW, Sridhar S, Zhang AJ, et al. Olfactory dysfunction in Coronavirus disease 2019 patients: observational cohort study and systematic review. Open Forum Infect Dis. 2020;7:ofaa199. PubMedPubMedCentralCrossRef Chung TW, Sridhar S, Zhang AJ, et al. Olfactory dysfunction in Coronavirus disease 2019 patients: observational cohort study and systematic review. Open Forum Infect Dis. 2020;7:ofaa199. PubMedPubMedCentralCrossRef
15.
Zurück zum Zitat Tong JY, Wong A, Zhu D, et al. The prevalence of olfactory and gustatory dysfunction in COVID-19 patients: a systematic review and meta-analysis. Otolaryngol Head Neck Surg. 2020;163:3. PubMedCrossRef Tong JY, Wong A, Zhu D, et al. The prevalence of olfactory and gustatory dysfunction in COVID-19 patients: a systematic review and meta-analysis. Otolaryngol Head Neck Surg. 2020;163:3. PubMedCrossRef
16.
Zurück zum Zitat Wang D, Hu B, Hu C, et al. Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. JAMA. 2020;323:1061. PubMedPubMedCentralCrossRef Wang D, Hu B, Hu C, et al. Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. JAMA. 2020;323:1061. PubMedPubMedCentralCrossRef
17.
Zurück zum Zitat Recalcati S. Cutaneous manifestations in COVID-19: a first perspective. J Eur Acad Dermatol Venereol. 2020;34:e212. PubMed Recalcati S. Cutaneous manifestations in COVID-19: a first perspective. J Eur Acad Dermatol Venereol. 2020;34:e212. PubMed
18.
Zurück zum Zitat Arentz M, Yim E, Klaff L, et al. Characteristics and outcomes of 21 critically ill patients with COVID-19 in Washington state. JAMA. 2020;323:1612. PubMedPubMedCentralCrossRef Arentz M, Yim E, Klaff L, et al. Characteristics and outcomes of 21 critically ill patients with COVID-19 in Washington state. JAMA. 2020;323:1612. PubMedPubMedCentralCrossRef
23.
Zurück zum Zitat Yang Z, Xu M, Yi JQ, Jia WD. Clinical characteristics and mechanism of liver damage in patients with severe acute respiratory syndrome. Hepatobiliary Pancreat Dis Int. 2005;4:60–3. PubMed Yang Z, Xu M, Yi JQ, Jia WD. Clinical characteristics and mechanism of liver damage in patients with severe acute respiratory syndrome. Hepatobiliary Pancreat Dis Int. 2005;4:60–3. PubMed
29.
Zurück zum Zitat LaRosa JC, He J, Vupputuri S. Effects of statins on risk of coronary artery disease: a meta-analysis of randomized controlled trials. JAMA. 1999;282:2340–6. PubMedCrossRef LaRosa JC, He J, Vupputuri S. Effects of statins on risk of coronary artery disease: a meta-analysis of randomized controlled trials. JAMA. 1999;282:2340–6. PubMedCrossRef
30.
Zurück zum Zitat Law MR, Wald NJ, Rudnicka AR. Quantifying effect of statins on low density lipoprotein cholesterol, ischaemic heart disease, and stroke: systemic review and meta-analysis. BMJ. 2003;326:1423. PubMedPubMedCentralCrossRef Law MR, Wald NJ, Rudnicka AR. Quantifying effect of statins on low density lipoprotein cholesterol, ischaemic heart disease, and stroke: systemic review and meta-analysis. BMJ. 2003;326:1423. PubMedPubMedCentralCrossRef
31.
Zurück zum Zitat Takemoto M, Liao JK. Pleiotropic effects of 3‑hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Arterioscler Thromb Vasc Biol. 2001;21:1712–9. PubMedCrossRef Takemoto M, Liao JK. Pleiotropic effects of 3‑hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Arterioscler Thromb Vasc Biol. 2001;21:1712–9. PubMedCrossRef
32.
Zurück zum Zitat Sacks FM, Pfeffer MA, Moye LA, Rouleau JL, Rutherford JD, Cole TG, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Engl J Med. 1996;335:1001–9. PubMedCrossRef Sacks FM, Pfeffer MA, Moye LA, Rouleau JL, Rutherford JD, Cole TG, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Engl J Med. 1996;335:1001–9. PubMedCrossRef
33.
Zurück zum Zitat Group TL-TIwPi. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med. 1998;339:1349–57. CrossRef Group TL-TIwPi. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med. 1998;339:1349–57. CrossRef
34.
Zurück zum Zitat Noma K, Oyama N, Liao JK. Physiological role of ROCKs in the cardiovascular system. Am J Physiol, Cell Physiol. 2006;290(16469861):C661–C8. CrossRef Noma K, Oyama N, Liao JK. Physiological role of ROCKs in the cardiovascular system. Am J Physiol, Cell Physiol. 2006;290(16469861):C661–C8. CrossRef
35.
Zurück zum Zitat Kataoka C, Egashira K, Inoue S, Takemoto M, Ni W, Koyanagi M, et al. Important role of Rho-kinase in the pathogenesis of cardiovascular inflammation and remodeling induced by long-term blockade of nitric oxide synthesis in rats. Hypertension. 2002;39:245–50. PubMedCrossRef Kataoka C, Egashira K, Inoue S, Takemoto M, Ni W, Koyanagi M, et al. Important role of Rho-kinase in the pathogenesis of cardiovascular inflammation and remodeling induced by long-term blockade of nitric oxide synthesis in rats. Hypertension. 2002;39:245–50. PubMedCrossRef
36.
Zurück zum Zitat Higashi M, Shimokawa H, Hattori T, Hiroki J, Mukai Y, Morikawa K, et al. Long-term inhibition of Rho-kinase suppresses angiotensin II-induced cardiovascular hypertrophy in rats in vivo: effect on endothelial NAD(P)H oxidase system. Circ Res. 2003;93:767–75. PubMedCrossRef Higashi M, Shimokawa H, Hattori T, Hiroki J, Mukai Y, Morikawa K, et al. Long-term inhibition of Rho-kinase suppresses angiotensin II-induced cardiovascular hypertrophy in rats in vivo: effect on endothelial NAD(P)H oxidase system. Circ Res. 2003;93:767–75. PubMedCrossRef
37.
Zurück zum Zitat Do EZ, Fukumoto Y, Sugimura K, et al. Rho-kinase activation in patients with heart failure. Circ J. 2013;77:2542–50. CrossRef Do EZ, Fukumoto Y, Sugimura K, et al. Rho-kinase activation in patients with heart failure. Circ J. 2013;77:2542–50. CrossRef
38.
Zurück zum Zitat Ohnaka K, Shimoda S, Nawata H, Shimokawa H, Kaibuchi K, Iwamoto Y, et al. Pitavastatin enhanced BMP‑2 and osteocalcin expression by inhibition of Rho-associated kinase in human osteoblasts. Biochem Biophys Res Commun. 2001;287:337–42. PubMedCrossRef Ohnaka K, Shimoda S, Nawata H, Shimokawa H, Kaibuchi K, Iwamoto Y, et al. Pitavastatin enhanced BMP‑2 and osteocalcin expression by inhibition of Rho-associated kinase in human osteoblasts. Biochem Biophys Res Commun. 2001;287:337–42. PubMedCrossRef
39.
Zurück zum Zitat Ma MM, Li SY, Wang M, Guan YY. Simvastatin attenuated cerebrovascular cell proliferation in the development of hypertension through Rho/Rho-kinase pathway. J Cardiovasc Pharmacol. 2012;59:576–82. PubMedCrossRef Ma MM, Li SY, Wang M, Guan YY. Simvastatin attenuated cerebrovascular cell proliferation in the development of hypertension through Rho/Rho-kinase pathway. J Cardiovasc Pharmacol. 2012;59:576–82. PubMedCrossRef
40.
Zurück zum Zitat Satoh M, Ogita H, Takeshita K, Mukai Y, Kwiatkowski DJ, Liao JK. Requirement of Rac1 in the development of cardiac hypertrophy. Proc Natl Acad Sci U S A. 2006;103:7432–7. PubMedPubMedCentralCrossRef Satoh M, Ogita H, Takeshita K, Mukai Y, Kwiatkowski DJ, Liao JK. Requirement of Rac1 in the development of cardiac hypertrophy. Proc Natl Acad Sci U S A. 2006;103:7432–7. PubMedPubMedCentralCrossRef
41.
Zurück zum Zitat Tanaka S, Fukumoto Y, Nochioka K, Minami T, Kudo S, Shiba N, et al. Statins exert the pleiotropic effects through small GTP-binding protein dissociation stimulator upregulation with a resultant Rac1 degradation. Arterioscler Thromb Vasc Biol. 2013;33:1591–600. PubMedCrossRef Tanaka S, Fukumoto Y, Nochioka K, Minami T, Kudo S, Shiba N, et al. Statins exert the pleiotropic effects through small GTP-binding protein dissociation stimulator upregulation with a resultant Rac1 degradation. Arterioscler Thromb Vasc Biol. 2013;33:1591–600. PubMedCrossRef
42.
Zurück zum Zitat Jones SP, Teshima Y, Akao M, Marban E. Simvastatin attenuates oxidant-induced mitochondrial dysfunction in cardiac myocytes. Circ Res. 2003;93:697–9. PubMedCrossRef Jones SP, Teshima Y, Akao M, Marban E. Simvastatin attenuates oxidant-induced mitochondrial dysfunction in cardiac myocytes. Circ Res. 2003;93:697–9. PubMedCrossRef
43.
Zurück zum Zitat Node K, Fujita M, Kitakaze M, Hori M, Liao JK. Short-term statin therapy improves cardiac function and symptoms in patients with idiopathic dilated cardiomyopathy. Circulation. 2003;108:839–43. PubMedPubMedCentralCrossRef Node K, Fujita M, Kitakaze M, Hori M, Liao JK. Short-term statin therapy improves cardiac function and symptoms in patients with idiopathic dilated cardiomyopathy. Circulation. 2003;108:839–43. PubMedPubMedCentralCrossRef
44.
Zurück zum Zitat Buber J, Goldenberg I, Moss AJ, Wang PJ, McNitt S, Hall WJ et al. Reduction in Life-Threatening Ventricular Tachyarrhythmias in Statin-Treated Patients With Nonischemic Cardiomyopathy Enrolled in the MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial with Cardiac Resynchronization Therapy). J Am Coll Cardiol. 2012;60:749–55. PubMedCrossRef Buber J, Goldenberg I, Moss AJ, Wang PJ, McNitt S, Hall WJ et al. Reduction in Life-Threatening Ventricular Tachyarrhythmias in Statin-Treated Patients With Nonischemic Cardiomyopathy Enrolled in the MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial with Cardiac Resynchronization Therapy). J Am Coll Cardiol. 2012;60:749–55. PubMedCrossRef
45.
Zurück zum Zitat Muhlhauser U, Zolk O, Rau T, Munzel F, Wieland T, Eschenhagen T. Atorvastatin desensitizes beta-adrenergic signaling in cardiac myocytes via reduced isoprenylation of G‑protein gamma-subunits. FASEB J. 2006;20:785–7. PubMedCrossRef Muhlhauser U, Zolk O, Rau T, Munzel F, Wieland T, Eschenhagen T. Atorvastatin desensitizes beta-adrenergic signaling in cardiac myocytes via reduced isoprenylation of G‑protein gamma-subunits. FASEB J. 2006;20:785–7. PubMedCrossRef
46.
Zurück zum Zitat Ridker PM, et al. Measurement of C‑reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events. N Engl J Med. 2001;344:1959–65. PubMedCrossRef Ridker PM, et al. Measurement of C‑reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events. N Engl J Med. 2001;344:1959–65. PubMedCrossRef
47.
48.
Zurück zum Zitat Diomede L, et al. In vivo anti-inflammatory effect of statins is mediated by nonsterol mevalonate products. Arterioscler Thromb Vasc Biol. 2001;21:1327–32. PubMedCrossRef Diomede L, et al. In vivo anti-inflammatory effect of statins is mediated by nonsterol mevalonate products. Arterioscler Thromb Vasc Biol. 2001;21:1327–32. PubMedCrossRef
49.
Zurück zum Zitat Stalker TJ, et al. A new HMG-CoA reductase inhibitor, rosuvastatin, exerts anti-inflammatory effects on the microvascular endothelium: the role of mevalonic acid. Br J Pharmacol. 2001;133:406–12. PubMedPubMedCentralCrossRef Stalker TJ, et al. A new HMG-CoA reductase inhibitor, rosuvastatin, exerts anti-inflammatory effects on the microvascular endothelium: the role of mevalonic acid. Br J Pharmacol. 2001;133:406–12. PubMedPubMedCentralCrossRef
50.
Zurück zum Zitat Liu L, et al. Integrin-dependent leukocyte adhesion involves geranylgeranylated protein(s). J Biol Chem. 1999;274:33334–40. PubMedCrossRef Liu L, et al. Integrin-dependent leukocyte adhesion involves geranylgeranylated protein(s). J Biol Chem. 1999;274:33334–40. PubMedCrossRef
51.
Zurück zum Zitat Takeuchi S, et al. Cerivastatin suppresses lipopolysaccharide-induced ICAM‑1 expression through inhibition of the rho GTPase in BAEC. Biochem Biophys Res Commun. 2000;269:97–102. PubMedCrossRef Takeuchi S, et al. Cerivastatin suppresses lipopolysaccharide-induced ICAM‑1 expression through inhibition of the rho GTPase in BAEC. Biochem Biophys Res Commun. 2000;269:97–102. PubMedCrossRef
52.
Zurück zum Zitat Inoue I, et al. Lipophilic HMG-CoA reductase inhibitor has an anti-inflammatory effect: Reduction of mRNAlevels for interleukin-1β, interleukin‑6, cyclooxygenase‑2, and p22phlox by regulation of peroxisome proliferator-activated receptor α(PPARα) in primary endothelial cells. Life Sci. 2000;67:863–76. PubMedCrossRef Inoue I, et al. Lipophilic HMG-CoA reductase inhibitor has an anti-inflammatory effect: Reduction of mRNAlevels for interleukin-1β, interleukin‑6, cyclooxygenase‑2, and p22phlox by regulation of peroxisome proliferator-activated receptor α(PPARα) in primary endothelial cells. Life Sci. 2000;67:863–76. PubMedCrossRef
54.
Zurück zum Zitat Grip O, et al. Atorvastatin activates PPAR-γand attenuates the inflammatory response in human monocytes. Inflamm Res. 2002;51:58–62. PubMedCrossRef Grip O, et al. Atorvastatin activates PPAR-γand attenuates the inflammatory response in human monocytes. Inflamm Res. 2002;51:58–62. PubMedCrossRef
55.
Zurück zum Zitat Zelvyte I, et al. Modulation of inflammatory mediators and PPARγand NFκB expression by pravastatin in response to lipoproteins in human monocytes in vitro. Pharmacol Res. 2002;45:147–54. PubMedCrossRef Zelvyte I, et al. Modulation of inflammatory mediators and PPARγand NFκB expression by pravastatin in response to lipoproteins in human monocytes in vitro. Pharmacol Res. 2002;45:147–54. PubMedCrossRef
56.
Zurück zum Zitat Laufs U, et al. Upregulation of endothelial nitric oxide synthase by HMG CoA reductase inhibitors. Circulation. 1998;97:1129–35. PubMedCrossRef Laufs U, et al. Upregulation of endothelial nitric oxide synthase by HMG CoA reductase inhibitors. Circulation. 1998;97:1129–35. PubMedCrossRef
57.
Zurück zum Zitat Ortego M, et al. Atorvastatin reduces NF-κB activation and chemokine expression in vascular smooth muscle cells and mononuclear cells. Atherosclerosis. 1999;147:253–61. PubMedCrossRef Ortego M, et al. Atorvastatin reduces NF-κB activation and chemokine expression in vascular smooth muscle cells and mononuclear cells. Atherosclerosis. 1999;147:253–61. PubMedCrossRef
65.
Zurück zum Zitat Trebicka J, Hennenberg M, Laleman W. et alAtorvastatin lowers portal pressure in cirrhotic rats byinhibition of RhoA/Rho-kinase and activation ofendothelial nitric oxide synthase. Hepatology. 2007;46:242–5. PubMedCrossRef Trebicka J, Hennenberg M, Laleman W. et alAtorvastatin lowers portal pressure in cirrhotic rats byinhibition of RhoA/Rho-kinase and activation ofendothelial nitric oxide synthase. Hepatology. 2007;46:242–5. PubMedCrossRef
67.
Zurück zum Zitat Watts KL, Sampson EM, Schultz GS, et al. Simvastatin inhibits growth factor expression and modulates profibrogenic markers in lung fibroblasts. Am J Respir Cell Mol Biol. 2005;32:290–300. PubMedCrossRef Watts KL, Sampson EM, Schultz GS, et al. Simvastatin inhibits growth factor expression and modulates profibrogenic markers in lung fibroblasts. Am J Respir Cell Mol Biol. 2005;32:290–300. PubMedCrossRef
68.
Zurück zum Zitat Nadrous HF, Ryu JH, Douglas WW, et al. Impact of angiotensin-converting enzyme inhibitors and statins on survival in idiopathic pulmonary fibrosis. Chest. 2004;126:438–46. PubMedCrossRef Nadrous HF, Ryu JH, Douglas WW, et al. Impact of angiotensin-converting enzyme inhibitors and statins on survival in idiopathic pulmonary fibrosis. Chest. 2004;126:438–46. PubMedCrossRef
69.
Zurück zum Zitat Meisel SR, Xu XP, Edgington TS, et al. Dose-dependent modulation of tissue factor protein andprocoagulantactivity in humanmonocyte-derived macrophagesbyoxidizedlowdensitylipoprotein. J Atheroscler Thromb. 2011;18(7):596–603. PubMedCrossRef Meisel SR, Xu XP, Edgington TS, et al. Dose-dependent modulation of tissue factor protein andprocoagulantactivity in humanmonocyte-derived macrophagesbyoxidizedlowdensitylipoprotein. J Atheroscler Thromb. 2011;18(7):596–603. PubMedCrossRef
75.
Zurück zum Zitat Rodriguez-Nava G, Trelles-Garcia DP, Yanez-Bello MA, Chung CW, Trelles-Garcia VP, Friedman HJ. Atorvastatin associated with decreased hazard for death in COVID-19 patients admitted to an ICU: a retrospective cohort study. Crit Care. 2020;24:429. PubMedPubMedCentralCrossRef Rodriguez-Nava G, Trelles-Garcia DP, Yanez-Bello MA, Chung CW, Trelles-Garcia VP, Friedman HJ. Atorvastatin associated with decreased hazard for death in COVID-19 patients admitted to an ICU: a retrospective cohort study. Crit Care. 2020;24:429. PubMedPubMedCentralCrossRef
Metadaten
Titel
The advantages of drug treatment with statins in patients with SARS-CoV-2 infection
verfasst von
Francesco Ferrara
Antonio Vitiello
Publikationsdatum
29.03.2021
Verlag
Springer Vienna
Erschienen in
Wiener klinische Wochenschrift / Ausgabe 17-18/2021
Print ISSN: 0043-5325
Elektronische ISSN: 1613-7671
DOI
https://doi.org/10.1007/s00508-021-01845-8

Weitere Artikel der Ausgabe 17-18/2021

Wiener klinische Wochenschrift 17-18/2021 Zur Ausgabe