Secular trends in hip fractures worldwide: opposing trends East versus West.

Despite wide variations in hip rates fractures worldwide, reasons for such differences are not clear. Furthermore, secular trends in the age-specific hip fracture rates are changing the world map of this devastating disease, with the highest rise projected to occur in developing countries. The aim of our investigation is to systematically characterize secular trends in hip fractures worldwide, examine new data for various ethnic groups in the United States, evidence for divergent temporal patterns, and investigate potential contributing factors for the observed change in their epidemiology. All studies retrieved through a complex Medline Ovid search between 1966 and 2013 were examined. For each selected study, we calculated the percent annual change in age-standardized hip fracture rates de-novo. Although occurring at different time points, trend breaks in hip fracture incidence occurred in most Western countries and Oceania. After a steep rise in age-adjusted rates in these regions, a decrease became evident sometimes between the mid-seventies and nineties, depending on the country. Conversely, the data is scarce in Asia and South America, with evidence for a continuous rise in hip fracture rates, with the exception of Hong-Kong and Taiwan that seem to follow Western trends. The etiologies of these secular patterns in both the developed and the developing countries have not been fully elucidated, but the impact of urbanization is at least one plausible explanation. Data presented here show close parallels between rising rates of urbanization and hip fractures across disparate geographic locations and cultures. Once the proportion of the urban population stabilized, hip fracture rates also stabilize or begin to decrease perhaps due to the influence of other factors such as birth cohort effects, changes in bone mineral density and BMI, osteoporosis medication use and/or lifestyle interventions such as smoking cessation, improvement in nutritional status and fall prevention.

Use of recombinant human parathyroid hormone in hypocalcemic cardiomyopathy.

Hypocalcemia secondary to hypoparathyroidism is a rare cause of congestive heart failure. However, its early recognition and treatment lead to significant improvement in cardiac function. We report a middle-aged woman presenting with symptoms of heart failure with a serum calcium level of 3.7 mg/dl and a serum inorganic phosphate level of 17.6 mg/dl 22 years after subtotal thyroidectomy. Besides calcium and calcitriol supplementation, she was the first patient with severe hypocalcemic cardiomyopathy to be given off-label recombinant human parathyroid hormone (PTH) because of an elevated serum calcium-phosphate product. We discuss the management and outcome of the patient and then present a brief review of similar previously reported cases. We also describe the pivotal role of calcium ion and the potential role of PTH in maintaining myocardial contractility, effective natriuresis, and possible pathogenic mechanisms contributing to heart failure secondary to hypocalcemia and hypoparathyroidism.

Myocardial perfusion in patients with a totally occluded left anterior descending coronary artery reinjected by a normal right coronary artery: the role of collateral circulation.

In this article, myocardial perfusion in patients with a totally occluded left anterior descending artery reinjected by a normal right coronary artery is assessed using stress single photon emission computed tomography (SPECT). In all, 20 patients, with a totally occluded left anterior descending artery reinjected by normal right coronary artery, underwent myocardial single photon emission computed tomography imaging within 60 days of angiography. All patients had abnormal perfusion single photon emission computed tomography results and 70% had reversible defects. Perfusion defects at rest were present in 75% of patients, with perinecrotic residual ischemia in 45% of patients whereas for 30% of patients, no viable myocardium was detected in the collateral-dependent segments. In all, 25% of patients had no resting perfusion defects but all are presented with stress-induced ischemia. Collaterals are not protective against stress-induced ischemia, but they can preserve myocardial viability. This conclusion is highly supported by the presence of residual ischemia in the collateral-dependent segments.