The temporal relationship of changes in atrial natriuretic peptide (ANP) secretion to other pathophysiological changes in heart failure has not been investigated. We studied the hemodynamic, hormonal, and metabolic changes before, during, and after the induction of heart failure in eight sheep using a 14-day period of rapid left ventricular pacing (LVP). Arterial pressure declined 21% on the first day, while cardiac output fell progressively to 48% of base line, and atrial pressures rose to a plateau over the first week. Plasma ANP levels increased 10-fold with a close correlation to left atrial pressure in all sheep. Furthermore, ANP secretion appeared to be sustained throughout the LVP period but did not prevent avid sodium retention. Marked and early activation of the renin-angiotensin system was observed, whereas the major increase in plasma aldosterone commenced 4 days later. On termination of LVP, a prompt natriuresis and diuresis occurred with return of all parameters toward base line. Thus this ovine model is useful for studying pathophysiological changes during the onset and offset of heart failure.

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Whether atrial natriuretic hormone (ANH) has biological effects at physiological plasma levels in man is not known. Accordingly, we investigated the effects of a 3-h low dose infusion of human ANF (0.75 pmol/kg.min; i.e. 0.0023 micrograms/kg.min) in six normal men, whose sodium intake was normal while sitting, in a single blind, random order, placebo-controlled study. The ANF infusions induced changes in plasma ANH concentrations entirely within the range for normal subjects. The small increases in plasma ANH values were associated with a significant rise in urinary excretion of sodium, magnesium, calcium, and cGMP. PRA and plasma aldosterone concentrations uniformly decreased to 50% and 64% of placebo values, respectively. Systolic and mean arterial pressures fell significantly from preinfusion values during the ANH infusions. These findings constitute strong evidence that ANH is a hormone of physiological significance in the regulation of body fluid volumes in normal man.

Background: TEXTMEDS (Text Messages to Improve Medication Adherence and Secondary Prevention After Acute Coronary Syndrome) examined the effects of text message–delivered cardiac education and support on medication adherence after an acute coronary syndrome. Methods: TEXTMEDS was a single-blind, multicenter, randomized controlled trial of patients after acute coronary syndrome. The control group received usual care (secondary prevention as determined by the treating clinician); the intervention group also received multiple motivational and supportive weekly text messages on medications and healthy lifestyle with the opportunity for 2-way communication (text or telephone). The primary end point of self-reported medication adherence was the percentage of patients who were adherent, defined as >80% adherence to each of up to 5 indicated cardioprotective medications, at both 6 and 12 months. Results: A total of 1424 patients (mean age, 58 years [SD, 11]; 79% male) were randomized from 18 Australian public teaching hospitals. There was no significant difference in the primary end point of self-reported medication adherence between the intervention and control groups (relative risk, 0.93 [95% CI, 0.84–1.03]; P =0.15). There was no difference between intervention and control groups at 12 months in adherence to individual medications (aspirin, 96% vs 96%; β-blocker, 84% vs 84%; angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, 77% vs 80%; statin, 95% vs 95%; second antiplatelet, 84% vs 84% [all P >0.05]), systolic blood pressure (130 vs 129 mm Hg; P =0.26), low-density lipoprotein cholesterol (2.0 vs 1.9 mmol/L; P =0.34), smoking ( P =0.59), or exercising regularly (71% vs 68%; P =0.52). There were small differences in lifestyle risk factors in favor of intervention on body mass index <25 kg/m 2 (21% vs 18%; P =0.01), eating ≥5 servings per day of vegetables (9% vs 5%; P =0.03), and eating ≥2 servings per day of fruit (44% vs 39%; P =0.01). Conclusions: A text message–based program had no effect on medical adherence but small effects on lifestyle risk factors. Registration: URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=364448 ; Unique identifier: ANZCTR ACTRN12613000793718.

The effects of renin inhibition have not previously been documented in established heart failure (HF). Accordingly, we investigated the acute hemodynamic and hormonal effects of a renin inhibitor (EMD 52297) in an ovine model of HF induced by rapid ventricular pacing (LVP). In seven sheep, recordings were made for 1 h before, during a 2-h infusion of renin inhibitor (RI) or vehicle, and after each infusion on the 5th and 6th day after commencing LVP. The RI (20 micrograms.kg-1.min-1) or vehicle was given in random order. RI infusion induced a rapid fall in plasma renin activity (PRA) and angiotensin II, reaching a nadir at 20 min. The vasodilator response was characterized by a 16% fall in mean arterial pressure (MAP), which was related to the fall in PRA (r = 0.78, P less than 0.05). MAP and PRA remained suppressed throughout the infusion period, and both returned to preinfusion levels within 10 min of terminating infusions. Left atrial pressure and plasma aldosterone were not significantly altered, while renal function was preserved despite the fall in perfusion pressure. RI has significant hemodynamic actions in a model of established HF.