Preoperative echocardiogram does not increase time to surgery in hip fracture patients with prior percutaneous coronary intervention.

BACKGROUND: The purpose of this study was to (1) assess the effect of preoperative echocardiogram on time to surgery and (2) assess the outcomes of patients with a previous percutaneous coronary intervention (PCI). METHODS: Demographic, clinical, quality and cost data were obtained and a validated risk predictive tool (STTGMA) was calculated for each of a consecutive series of hip fracture patients. Comparative analyses of patients who had an echocardiogram prior to surgery or a PCI prior to hospitalization were performed. RESULTS: Between 2014 and 2020, 2625 patients presented to our institution with a hip fracture. From this cohort 471 patients underwent a preoperative transthoracic echocardiogram (TTE), 30 who had a history of a PCI, and an additional 26 who had a history of PCI but did not undergo a preoperative TTE. Those undergoing a preoperative TTE had similar time (days) to surgery (1.73 vs 1.77, p = 0.86) and 30-day mortality (4% vs 7%, p = 0.545) regardless of PCI history. PCI patients who underwent a preoperative TTE experienced increased rates of 1-year mortality (27% vs 10%, p = 0.007) and major complications (23% vs 12%, p = 0.08) compared to those without a PCI history. PCI patients undergoing a preoperative TTE had a similar time (days) to surgery (1.77 vs 1.48, .p = 0.397) compared to PCI patients without a preoperative TTE. Patients who underwent a preoperative TTE had higher rates of 90-day readmission (31.0% vs 8.0%, p = 0.047) and 1-year mortality (26.7% vs 3.8%, p = 0.029). CONCLUSIONS: Having a preoperative TTE does not affect surgical wait times in hip fracture patients regardless of PCI history, but it may not improve mortality outcomes or reduce postoperative complications in patients with a history of a PCI.

Occult double RV physiology complicating VSD repair.

Double-chamber right ventricle (DCRV) is an uncommon congenital abnormality usually described in children. It occurs due to partitioning of the right ventricle by prominent muscle bundles. In this case report, we describe an adult in cardiogenic shock postoperatively from repair of a ventricular septal defect in whom a previously undiagnosed DCRV was found to be clinically significant.

Increase in circulating bone marrow progenitor cells after myocardial infarction.

BACKGROUND: Most circulating blood cells expressing the marker CD34 are bone marrow progenitor cells. These cells differentiate into cardiomyocytes, endothelial and smooth muscle cells after myocardial infarction in vivo. Mobilization of bone marrow progenitor cells into the peripheral blood after myocardial infarction may supply these cells to the heart. Rise in CD34+ cell concentrations following myocardial infarction would support the existence of myocardial-initiated mobilization. METHODS: Serial measurements of circulating CD34+ cells were made in 42 consecutive patients presenting with first ST-elevation myocardial infarction. Measurement of serum concentrations of monocyte chemoattractant protein-1, stromal derived factor-1, hepatocyte growth factor, interleukin-17 and thrombopoietin was also performed. Samples were drawn on day 1 after myocardial infarction, and on days 4, 8 and 12. Levels of CD34+ cells and cytokines were also measured in 15 controls. RESULTS: By day 8, the mean concentration of CD34+ cells rose by 74% above mean control level of 2527 cells/ml, and 41% above day 1 mean (P=0.02). This rise was sustained on day 12 (P=0.05). On day 1, there was a 9.3-fold rise in hepatocyte growth factor above the control level of 589 pg/ml (P=0.002). Hepatocyte growth factor levels declined from the day 1 mean of 6061 to 1485 pg/ml on day 12 (P=0.002). No significant change in stromal derived factor-1, interleukin-17, monocyte chemoattractant protein-1 and thrombopoietin was observed. Elevations in CD34+ cells and hepatocyte growth factor were not related to infarction size as estimated on echocardiography. CONCLUSIONS: Elevation in the concentration of circulating CD34+ cells after myocardial infarction suggests that myocardial initiated bone marrow progenitor cell mobilization exists in humans. The cytokines studied in our protocol are not likely to play a direct role in bone marrow progenitor cell mobilization.