Incidence of Left Ventricular Thrombus in Patients With Acute ST-Segment Elevation Myocardial Infarction Treated with Percutaneous Coronary Intervention.

Previous studies using 2-dimensional non-contrast echocardiography have reported a post-ST segment elevation myocardial infarction (STEMI) left ventricular (LV) thrombus incidence of 3% to 24%. However, these studies were not performed with ultrasound contrast agents (UCAs), which improve accuracy in the diagnosis of LV thrombus. We aimed to determine the early incidence and clinical correlates of LV thrombus in a large consecutive cohort of patients with STEMI. This study included consecutive patients admitted to Saint Luke's Mid America Heart Institute with STEMI who also underwent early percutaneous coronary intervention (PCI) and an echocardiogram. A total of 1,698 patients (1,205 men, mean age 61 ± 13 years) comprised the study group. Echocardiography was performed on hospital day 2, and a UCA was used in 1,292 patients (76%). LV thrombus was identified in 28 (1.6%) patients. A multivariable logistic regression model showed that left anterior descending intervention was independently associated with LV thrombus (odds ratio = 7.58, 95% confidence interval [CI] 2.20 to 26.19, p = 0.001), thrombolysis in myocardial infarction III flow was marginally associated with less LV thrombus (odds ratio = 0.41, 95% CI 0.16 to 1.04, p = 0.060), and higher LVEF was associated with less LV thrombus (odds ratio = 0.96, 95% CI 0.91 to 0.97, p <0.001). In conclusion, LV thrombus was identified in only 1.6% of patients in a large STEMI cohort, significantly lower than previous studies. A UCA was used in most echocardiograms, and it improves accuracy in the detection and exclusion of LV thrombus.

FGF23 is a novel regulator of intracellular calcium and cardiac contractility in addition to cardiac hypertrophy.

Fibroblast growth factor 23 (FGF23) is a hormone released primarily by osteocytes that regulates phosphate and vitamin D metabolism. Recent observational studies in humans suggest that circulating FGF23 is independently associated with cardiac hypertrophy and increased mortality, but it is unknown whether FGF23 can directly alter cardiac function. We found that FGF23 significantly increased cardiomyocyte cell size in vitro, the expression of gene markers of cardiac hypertrophy, and total protein content of cardiac muscle. In addition, FGFR1 and FGFR3 mRNA were the most abundantly expressed FGF receptors in cardiomyocytes, and the coreceptor α-klotho was expressed at very low levels. We tested an animal model of chronic kidney disease (Col4a3(-/-) mice) that has elevated serum FGF23. We found elevations in common hypertrophy gene markers in Col4a3(-/-) hearts compared with wild type but did not observe changes in wall thickness or cell size by week 10. However, the Col4a3(-/-) hearts did show reduced fractional shortening (-17%) and ejection fraction (-11%). Acute exposure of primary cardiomyocytes to FGF23 resulted in elevated intracellular Ca(2+) ([Ca(2+)](i); F/F(o) + 86%) which was blocked by verapamil pretreatment. FGF23 also increased ventricular muscle strip contractility (67%), which was inhibited by FGF receptor antagonism. We hypothesize that although FGF23 can acutely increase [Ca(2+)](i), chronically this may lead to decreases in contractile function or stimulate cardiac hypertrophy, as observed with other stress hormones. In conclusion, FGF23 is a novel bone/heart endocrine factor and may be an important mediator of cardiac Ca(2+) regulation and contractile function during chronic kidney disease.