Long-term blood pressure changes induced by the 2009 L'Aquila earthquake: assessment by 24 h ambulatory monitoring.

An increased rate of cardiovascular and cerebrovascular events has been described during and immediately after earthquakes. In this regard, few data are available on long-term blood pressure control in hypertensive outpatients after an earthquake. We evaluated the long-term effects of the April 2009 L'Aquila earthquake on blood pressure levels, as detected by 24 h ambulatory blood pressure monitoring. Before/after (mean±s.d. 6.9±4.5/14.2±5.1 months, respectively) the earthquake, the available 24 h ambulatory blood pressure monitoring data for the same patients were extracted from our database. Quake-related daily life discomforts were evaluated through interviews. We enrolled 47 patients (25 female, age 52±14 years), divided into three groups according to antihypertensive therapy changes after versus before the earthquake: unchanged therapy (n=24), increased therapy (n=17) and reduced therapy (n=6). Compared with before the quake, in the unchanged therapy group marked increases in 24 h (P=0.004), daytime (P=0.01) and nighttime (P=0.02) systolic blood pressure were observed after the quake. Corresponding changes in 24 h (P=0.005), daytime (P=0.01) and nighttime (P=0.009) diastolic blood pressure were observed. Daily life discomforts were reported more frequently in the unchanged therapy and increased therapy groups than the reduced therapy group (P=0.025 and P=0.018, respectively). In conclusion, this study shows that patients with unchanged therapy display marked blood pressure increments up to more than 1 year after an earthquake, as well as long-term quake-related discomfort. Our data suggest that particular attention to blood pressure levels and adequate therapy modifications should be considered after an earthquake, not only early after the event but also months later.

Electrophysiological effects of short-term antihypertensive therapy.

Left ventricular hypertrophy (LVH) detected by ECG has been shown to be associated with a higher prevalence of ventricular arrhythmias in members of the general population, in a case-control series of hypertensive patients and in never-treated hypertensive patients. In-keeping with this, it has been observed that hypertension-induced LVH increases the risk of sudden cardiac death. Furthermore, a consistent bulk of data suggests antihypertensive therapy targeted at regression or prevention of electrocardiographic LVH may reduce the incidence of arrhythmias. In this regard, recent clinical trials showed that antihypertensive therapy may delay or prevent the occurrence of cardiac arrhythmias and sudden cardiac death in patients with hypertension. Porthan et al. hypothesized that an antihypertensive therapy might also rapidly affect ventricular repolarization and sought to investigate the short-term electrophysiological effects of four common antihypertensive drugs, represented by an angiotensin II receptor blocker (losartan), a beta-blocker (bisoprolol), a calcium channel blocker (amlodipine) and a thiazide diuretic (hydrochlorothiazide) in hypertensive men. Porthan et al. showed that losartan and bisoprolol favorably affected ventricular repolarization, with beneficial effects on ECG parameters of ventricular repolarization duration and heterogeneity. On the contrary, hydrochlorothiazide significantly increased repolarization heterogeneity, while amlodipine administration did not affect ECG repolarization measures. Thus, the observed findings suggest an intriguing hypothesis on the possible role of antihypertensive therapy in favouring or preventing cardiac arrhythmias.

Cocoa reduces blood pressure and insulin resistance and improves endothelium-dependent vasodilation in hypertensives.

Consumption of flavanol-rich dark chocolate (DC) has been shown to decrease blood pressure (BP) and insulin resistance in healthy subjects, suggesting similar benefits in patients with essential hypertension (EH). Therefore, we tested the effect of DC on 24-hour ambulatory BP, flow-mediated dilation (FMD), and oral glucose tolerance tests (OGTTs) in patients with EH. After a 7-day chocolate-free run-in phase, 20 never-treated, grade I patients with EH (10 males; 43.7+/-7.8 years) were randomized to receive either 100 g per day DC (containing 88 mg flavanols) or 90 g per day flavanol-free white chocolate (WC) in an isocaloric manner for 15 days. After a second 7-day chocolate-free period, patients were crossed over to the other treatment. Noninvasive 24-hour ambulatory BP, FMD, OGTT, serum cholesterol, and markers of vascular inflammation were evaluated at the end of each treatment. The homeostasis model assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), and insulin sensitivity index (ISI) were calculated from OGTT values. Ambulatory BP decreased after DC (24-hour systolic BP -11.9+/-7.7 mm Hg, P<0.0001; 24-hour diastolic BP -8.5+/-5.0 mm Hg, P<0.0001) but not WC. DC but not WC decreased HOMA-IR (P<0.0001), but it improved QUICKI, ISI, and FMD. DC also decreased serum LDL cholesterol (from 3.4+/-0.5 to 3.0+/-0.6 mmol/L; P<0.05). In summary, DC decreased BP and serum LDL cholesterol, improved FMD, and ameliorated insulin sensitivity in hypertensives. These results suggest that, while balancing total calorie intake, flavanols from cocoa products may provide some cardiovascular benefit if included as part of a healthy diet for patients with EH.