Dual antiplatelet agents and high-intensity statins are frequently used in combination after myocardial infarction. Ticagrelor has the potential of causing acute kidney injury. Rosuvastatin is excreted through the kidneys and dose adjustment is needed in patients with kidney disease. When used in combination, they can potentiate the toxic effects of each other. We report a case of drug interaction between rosuvastatin and ticagrelor resulting in rhabdomyolysis and acute renal failure necessitating dialysis. This case stresses the importance of monitoring renal function and adjusting the dose of rosuvastatin accordingly in patients with kidney disease.

Contrast-induced acute kidney injury (CI-AKI) is a common complication of many diagnostic and therapeutic cardiovascular procedures. It is associated with longer in-hospital stay, more complicated hospitalization course, and higher in-hospital morbidity and mortality. With increasing use of contrast media in various diagnostic and interventional procedures, the prevalence of CI-AKI is expected to rise. Although pre-hydration with intravenous normal saline is recommended in patients with elevated risk of CI-AKI, this approach is often not feasible in many clinical settings. Remote ischemic conditioning (RIC), elicited by application of one or more, brief, non-injurious episodes of ischemia and reperfusion of a limb, is a promising therapy for preventing or attenuating the deleterious effects of contrast media on the kidney. Although the mechanisms of protection by RIC have not been completely defined, complex humoral, neural, and inflammatory pathways have been hypothesized to be in play. Given that RIC is non-invasive and cheap, it is attractive from clinical and economic perspective as a therapy to protect the kidney from CI-AKI. In this succinct review, we highlight the unifying mechanisms of CI-AKI and provide an overview of proposed biological mechanisms of renal protection by RIC. Emerging pre-clinical and clinical evidence in interventional cardiology are also discussed.

Background: Few studies have examined the relationship between heavy metal and serum cholesterol levels, and no recent study has examined this relationship in the US population. Methods and Results: A total of 19,591 individuals aged 0–80 years were included in the National Health and Nutrition Examination Survey 2009–2012; the current study was composed of survey participants for whom some or all low-density lipoprotein cholesterol (LDL-C), serum triglyceride, high-density lipoprotein cholesterol, total cholesterol, blood lead (Pb), total blood mercury (Hg), and blood cadmium (Cd) levels had been measured. Three tertiles (T1–T3) of heavy metals were used to explore dose–response association between heavy metal exposure and serum cholesterol level. Logistic regression was used to explore the relationship between tertiles of blood heavy metal levels and serum cholesterol levels after adjusting for age, sex, and socioeconomic status. We have shown that the groups with the highest levels of Pb, Hg, and Cd had a 56%, 73%, and 41% chance, respectively, of having a high total cholesterol level. In study subjects with the highest Pb levels, there was also a 22% chance of being in the group with the highest LDL-C level. An increase in total cholesterol and LDL-C levels was observed from the first to the third tertiles of the heavy metals studied. Conclusion: Increasing blood Pb, Hg, and Cd levels were associated with significantly increased odds of high total cholesterol after adjusting for age, sex, and socioeconomic status.

Sickle cell disease (SCD) predominantly affects African-Americans (AAs) in the United States (US). Due to increasing life expectancy in developed countries, SCD-associated cardiomyopathy is typically seen in adults. The aim of this study was to distinguish hospitalization for this phenotype from traditional heart failure (HF) in AAs. We used the National Inpatient Sample (NIS) database to identify HF hospitalizations in AAs between 2005 and 2014 and stratified them according to SCD status. We compared the characteristics and outcomes before and after matching in a 1:3 ratio for age, gender, insurance, smoking status and admission year. Amongst the 1,195,718 HF admissions in AAs, SCD accounted for 7835. The age (mean ± SD) in the SCD cohort was significantly younger (45.66 ± 13.2) vs non-SCD (64.8 ± 15.2), p<0.001. SCD adults had significantly higher rates of pulmonary hypertension (PH), deep vein thrombosis, and pulmonary embolism while non-SCD adults had higher rates of cardiogenic shock and respiratory failure requiring intubation. The national hospitalization rate for HF in AAs increased from 151 to 257 per million between 2005 and 2011 before declining to 241 per million in 2014. There was a decrease in in-hospital mortality in AAs from 4.8% in 2005 to 3.6% in 2014. We also identified independent predictors of in-hospital mortality in SCD with HF. In conclusion, we described hospitalizations for an emerging heart failure phenotype in AAs. Although there is a national decreasing rate of HF hospitalizations in the US, this may not be reflective of the AA population.

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