Abstract
BackgroundTo assess whether a banking system crisis increases short-term population cardiovascular mortality rates.MethodsInternational, longitudinal multivariate regression analysis of cardiovascular disease mortality data from 1960 to 2002ResultsA 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.ConclusionBanking crises are a significant determinant of short-term increases in heart disease mortality rates, and may have more severe consequences for developing countries.
Highlights
To assess whether a banking system crisis increases short-term population cardiovascular mortality rates
The spread of panic, in part propelled by media, appears to have turned what could have otherwise been a momentary blip on the financial scene into an economic policy debacle – leading to a reluctant intervention by the Bank of England and an historic guarantee by the chancellor of the exchequer of all Northern Rock deposits in the UK banking system
Since bank crises often last for multiple years, indicators are used for the first year of a country's banking system crisis in order to isolate the short-term effect on mortality
Summary
To assess whether a banking system crisis increases short-term population cardiovascular mortality rates. As the runs on Northern Rock banks in England took place, one could not help but wonder how people's trust in the financial system could have eroded so rapidly.. As the current experiences suggest, banking crises impose considerable panic and stress on people and, in particular, on vulnerable older populations. Such acute mental distress has been shown to i) significantly raise heart rate and blood pressure, which may increase myocardial oxygen demand and disrupt vulnerable plaques, and ii) in atherosclerotic patients lead to primary reductions in myocardial oxygen supply via impaired dilatation and vasoconstriction [1,2,3,4]. Clinical and experimental studies have documented that extremely stressful events, such as earthquakes [5], wars [6] or terrorist attacks [7,8] are associated with increased risk of acute myocardial infarction and sudden cardiac death
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