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Objective Studies have related air pollution to myocardial infarction (MI) events over days or weeks, with few data on very short-term risks. We studied risk of ST-segment elevation MI (STEMI) within hours of exposure to air pollution while adjusting for weather. Methods We performed a case-crossover study of STEMI cases in Stockholm, Sweden (Jan 2000–June 2014) based on SWEDEHEART. Exposures during hazard periods up to 24 h prior to admission were compared to bidirectionally sampled control periods. Risks attributable to sulphur dioxide (SO2), nitrogen dioxide (NO2), ozone and particulate pollutants (PM2.5, PM10) were studied in conditional logistic regression models for interquartile range increments. Results Risk of STEMI (n = 14,601) was associated with NO2 (strongest at 15-h lag) and with PM2.5 (strongest at 20-h lag), in single-pollutant models adjusting for air temperature and humidity (NO2: odds ratio (OR; 95% confidence interval) 1.065 (1.031–1.101); PM2.5: 1.026 (1.001–1.054)). After adjusting models for atmospheric pressure (significantly associated with STEMI risk at 14–24-h lags), NO2 remained highly statistically significant (1.057 (1.022–1.094)) but not PM2.5 (1.024 (0.997–1.052)). No associations were seen for SO2, ozone or PM10. Conclusion Risk of STEMI rises within hours of exposure to air pollutants, with strongest impact of NO2. These findings are complementary to earlier reports which have not acknowledged widely the importance of very short-term fluctuations in air pollution.

The ratio of the early transmitral flow velocity to the early diastolic tissue velocity (E/Em) has been suggested as a reliable estimate of left ventricular diastolic pressures (LVDP). However, the evidence regarding the ability of E/Em to detect LVDP changes is relatively equivocal. Our aim was to evaluate the validity of the ratio following acute load reduction.68 consecutive patients referred for coronary angiography underwent LV catheterization and echocardiography simultaneously. Doppler signals of transmitral flow and spectral TD signals at the level of the mitral annulus were obtained before and directly after intravenous administration of nitroglycerin (NTG). The predictive ability of E/Em to identify elevated LVDP was modest (area under curve=0.71 ± 0.08, p0.01). The index was more strongly associated with LVDP in patients with reduced ejection fraction (EF)55% (r=0.68; p0.01) than in patients with normal EF. Following NTG, E/Em lacked any predictive potential for elevated LVDP whereas changes LVDP could not be reliably tracked using E/Em.The predictive capacity of E/Em for elevated LVDP was weak and declined significantly following acute reduction in LV load. Changes in LVDP were not reliably predicted by E/Em. The current findings derived from a real-world patient population with relatively high filling pressures indicate that E/Em may not be sufficiently robust to be employed as a single non-invasive estimate of LVDP nor for monitoring load reducing medical therapy.