Response to therapy with tafamidis 61 mg in patients with cardiac transthyretin amyloidosis: real-world experience since approval.

AIMS: Transthyretin amyloid cardiomyopathy (ATTR-CM) is a progressive disease that causes heart failure due to amyloid fibril deposition. Tafamidis was approved as the first causal treatment in 2020. We here report on real-world data in patients treated with tafamidis for at least 12 months according to the recently defined European Society for Cardiology (ESC) consensus criteria for disease progression. METHODS AND RESULTS: Three hundred and eight wildtype and 31 hereditary ATTR-CM patients were prospectively enrolled after first diagnosis of ATTR-CM and initiation of tafamidis 61 mg once daily treatment. After 12 months, significant deterioration in Karnofsky Index, estimated glomerular filtration rate (eGFR), N-terminal brain natriuretic peptide (NT-proBNP), septum thickness and left ventricular ejection fraction (LVEF) could be observed, significant disease progression was only detected in 25 patients (9%) using ESC consensus criteria. Mean survival time was 37 months with no differences between responders and non-responders. NT-proBNP was the only independent predictor for poor therapy response (p = .008). CONCLUSIONS: The majority of patients showed no significant disease progression according to the ESC consensus criteria after 12 months of therapy with tafamidis. However, at 12 months, treatment response based on the ESC consensus criteria was not associated with improved survival. Moreover, higher levels of NT-proBNP at diagnosis of ATTR-CM appears to predict poorer treatment response, confirming that timely initiation of therapy is advantageous.

Persistent Pandemics.

We ask whether mortality from historical pandemics has any predictive content for mortality in the Covid-19 pandemic. We find strong persistence in public health performance. Places that performed worse in terms of mortality in the 1918 influenza pandemic also have higher Covid-19 mortality today. This is true across countries as well as across a sample of large US cities. Experience with SARS in 2003 is associated with slightly lower mortality today. We discuss some socio-political factors that may account for persistence including distrust of expert advice, lack of cooperation, over-confidence, and health care supply shortages. Multi-generational effects of past pandemics may also matter.

Does investment in the health sector promote or inhibit economic growth?

BACKGROUND: Is existing provision of health services in Europe affordable during the recession or could cuts damage economic growth? This debate centres on whether government spending has positive or negative effects on economic growth. In this study, we evaluate the economic effects of alternative types of government spending by estimating "fiscal multipliers" (the return on investment for each $1 dollar of government spending). METHODS: Using cross-national fixed effects models covering 25 EU countries from 1995 to 2010, we quantified fiscal multipliers both before and during the recession that began in 2008. RESULTS: We found that the multiplier for total government spending was 1.61 (95% CI: 1.37 to 1.86), but there was marked heterogeneity across types of spending. The fiscal multipliers ranged from -9.8 for defence (95% CI: -16.7 to -3.0) to 4.3 for health (95% CI: 2.5 to 6.1). These differences appear to be explained by varying degrees of absorption of government spending into the domestic economy. Defence was linked to significantly greater trade deficits (ß = -7.58, p=0.017), whereas health and education had no effect on trade deficits (peducation=0.62; phealth= 0.33). CONCLUSION: Our findings indicate that government spending on health may have short-term effects that make recovery more likely.

Banking crises and mortality during the Great Depression: evidence from US urban populations, 1929-1937.

BACKGROUND: Previous research suggests that the Great Depression led to improvements in public health. However, these studies rely on highly aggregated national data (using fewer than 25 data points) and potentially biased measures of the Great Depression. The authors assess the effects of the Great Depression using city-level estimates of US mortality and an underlying measure of economic crisis, bank suspensions, at the state level. METHODS: Cause-specific mortalities covering 114 US cities in 36 states between 1929 and 1937 were regressed against bank suspensions and income data from the Federal Deposit Insurance Corporation Database, using dynamic fixed-effects models and adjustments for potential confounding variables. RESULTS: Reductions in all-cause mortalities were mainly attributable to declines in death rates owing to pneumonia (26.4% of total), flu (13.1% of total) and respiratory tuberculosis (11.2% of total), while death rates increased from heart disease (19.4% of total), cancer (8.1% of total) and diabetes (2.9%). Only heart disease can plausibly relate to the contemporaneous economic shocks. The authors found that a higher rate of bank suspensions was significantly associated with higher suicide rates (ß=0.32, 95% CI 0.24 to 0.41) but lower death rates from motor-vehicle accidents (ß=-0.18, 95% CI -0.29 to -0.07); no significant effects were observed for 30 other causes of death or with a time lag. CONCLUSION: In contrast with existing research, the authors find that many of the changes in deaths from different causes during the Great Depression were unrelated to economic shocks. Further research is needed to understand the causes of the marked variations in mortality change across cities and states, including the effects of the New Deal and Prohibition.

Can a bank crisis break your heart?

BACKGROUND: To assess whether a banking system crisis increases short-term population cardiovascular mortality rates. METHODS: International, longitudinal multivariate regression analysis of cardiovascular disease mortality data from 1960 to 2002 RESULTS: A system-wide banking crisis increases population heart disease mortality rates by 6.4% (95% CI: 2.5% to 10.2%, p < 0.01) in high income countries, after controlling for economic change, macroeconomic instability, and population age and social distribution. The estimated effect is nearly four times as large in low income countries. CONCLUSION: Banking crises are a significant determinant of short-term increases in heart disease mortality rates, and may have more severe consequences for developing countries.