1,721,041 research outputs found
From microvascular impairment to cardiac allograft vasculopathy: A disease continuum
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Effect of coenzyme Q10 therapy in patients with congestive heart failure: a long-term multicenter randomized study
No full textThe improved cardiac function in patients with congestive heart failure treated with coenzyme Q10 supports the hypothesis that this condition is characterized by mitochondrial dysfunction and energy starvation, so that it may be ameliorated by coenzyme Q10 supplementation. However, the main clinical problems in patients with congestive heart failure are the frequent need of hospitalization and the high incidence of life-threatening arrhythmias, pulmonary edema, and other serious complications. Thus, we studied the influence of coenzyme Q10 long-term treatment on these events in patients with chronic congestive heart failure (New York Heart Association functional class III and IV) receiving conventional treatment for heart failure. They were randomly assigned to receive either placebo (n = 322, mean age 67 years, range 30-88 years) or coenzyme Q10 (n = 319, mean age 67 years, range 26-89 years) at the dosage of 2 mg/kg per day in a 1-year double-blind trial. The number of patients who required hospitalization for worsening heart failure was smaller in the coenzyme Q10 treated group (n = 73) than in the control group (n = 118, P < 0.001). Similarly, the episodes of pulmonary edema or cardiac asthma were reduced in the control group (20 versus 51 and 97 versus 198, respectively; both P < 0.001) as compared to the placebo group. Our results demonstrate that the addition of coenzyme Q10 to conventional therapy significantly reduces hospitalization for worsening of heart failure and the incidence of serious complications in patients with chronic congestive heart failure. © 1993 Springer-Verlag
The rationale for angiotensin receptor neprilysin inhibitors in a multi-targeted therapeutic approach to COVID-19
Full text linkThe severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) determines the angiotensin converting enzyme 2 (ACE2) down-regulation and related decrease in angiotensin II degradation. Both these events trigger “cytokine storm” leading to acute lung and cardiovascular injury. A selective therapy for COVID-19 has not yet been identified. Clinical trials with remdesivir gave discordant results. Thus, healthcare systems have focused on “multi-targeted” therapeutic strategies aiming at relieving systemic inflammation and thrombotic complications. No randomized clinical trial has demonstrated the efficacy of renin angiotensin system antagonists in reducing inflammation related to COVID-19. Dexamethasone and tocilizumab showed encouraging data, but their use needs to be further validated. The still-controversial efficacy of these treatments highlighted the importance of organ injury prevention in COVID-19. Neprilysin (NEP) might be an interesting target for this purpose. NEP expression is increased by cytokines on lung fibroblasts surface. NEP activity is elevated in acute respiratory distress syndrome and it is conceivable that it is also high in COVID-19. NEP is implicated in the degradation of natriuretic peptides, bradykinin, substance P, adrenomedullin, and apelin that account for prevention of organ injury. Thus, NEP/angiotensin receptor type 1 (AT1R) inhibitor sacubitril/valsartan (SAC/VAL) may increase levels of these molecules and block AT1Rs required for ACE2 endocytosis in SARS-CoV-2 infection. Moreover, SAC/VAL has a positive impact on acute heart failure that is very frequently observed in deceased COVID-19 patients. The current review aims to summarize actual therapeutic strategies for COVID-19 and to examine the data supporting the potential benefits of SAC/VAL in COVID-19 treatment
The PARADISE-MI trial. a new opportunity to improve the left ventricular remodelling in reperfused STEMI
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PCSK9 Inhibitors: Is the Time Ripe for the “Fast Track” Use Independently on the LDL-C Baseline Values in Acute Coronary Syndrome?
Full text link: The low-density lipoprotein cholesterol (LDL-C) lowering decreases the risk to develop major adverse cardiovascular events (MACE) in patients with acute coronary syndrome (ACS). Therefore, the "fast track" use of PCSK9 inhibitors (PCSK9i) has been introduced in ACS patients not achieving LDL-C target (70 mg/dl) despite an ongoing lipid lowering therapy with statin at maximum tolerated dosage plus ezetimibe or stain-naïve (LDL-C > 130 mg/dl). PCSK9i "fast track" use has shown to achieve the regression of "non-culprit" atherosclerotic plaques leading to a further MACE decrease. Interestingly, it has been also hypothesized a role of PCSK9i beyond the LDL-C lowering in ACS. PCSK9i have been demonstrated to decrease the inflammation of atherosclerotic plaques and myocardium, inhibit platelet aggregation, and improve the cardiomyocyte survival against the reperfusion injury. All these findings may positively impact on the prognosis and suggest the PCSK9i use in the acute phase of ACS independently on the baseline LDL-C values
Spontaneous coronary artery dissection in a young woman with polycystic ovarian syndrome
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Paradoxical insulin-like growth factor-1 effect on aortic rings from spontaneously hypertensive rats
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