Does subjective evaluation of the frequency of salty food intake predict the risk of incident hypertension? A 4-year follow-up study in a middle-aged population.

BACKGROUND: Excess salt intake increases blood pressure (BP). Identifying individuals with excess salt intake is, therefore, important for the prevention of hypertension. AIM: To examine the predictive value of subjective evaluation of salty foods intake for the risk of incident hypertension in a middle-aged population. METHODS: A total of 970 non-hypertensive workers (mean age, 44 ± 6 years) was followed for a maximum period of 4 years, and their BP was measured annually. At baseline, all participants were asked about their subjective frequency of salty foods intake (seldom, sometimes or always), and they were divided into three groups according to their answers. Hypertension was defined as systolic/diastolic BP ≥ 140/90 mmHg or use of antihypertensive medications. RESULTS: There were no significant differences in the 4-year cumulative incident rate of hypertension among the 'seldom', 'sometimes' and 'always' groups (15.8%, 14.3% and 10.3%, respectively, log-rank test P = 0.44). In a multivariate Cox proportional hazards model, age, body mass index and the baseline BP category were independent predictors for developing hypertension, whereas the frequency of salty foods intake was not a predictor (adjusted hazard ratio (95% confidence interval), 0.99 (0.64-1.54) in the 'sometimes' group and 0.64 (0.33-1.28) in the 'always' group as compared with the 'seldom' group). CONCLUSION: The subjective evaluation of salty foods intake did not predict the 4-year risk of incident hypertension in this study population. Further investigations with a longer follow-up period are needed to clarify whether the present insignificant results are maintained for more than 4 years.

Effects of acidic reperfusion on arrhythmias and Na(+)-K(+)-ATPase activity in regionally ischemic rat hearts.

We studied the effects of acidic reperfusion on 1) the incidence of ventricular fibrillation (VF) and 2) sarcolemmal Na(+)-K(+)-adenosinetriphosphatase (ATPase) activity. Isolated rat hearts (n = 12/group) were subjected to independent perfusion (15 min) of left and right coronary beds with pH 7.4 buffer followed by zero-flow ischemia (10 min) of the former bed. This was then reperfused for 5 min, with acidic (pH 6.6) buffer for the first 0 (control), 0.5,1,2, or 4 min and with pH 7.4 buffer thereafter. In the control group, 92% of hearts developed VF within 20 s of reperfusion and remained in VF. In the 0.5-, 1-, 2-, and 4-min acidic reperfusion groups, only 17, 17, 42, and 25% of hearts (P < 0.05 vs. control for all groups), respectively, exhibited VF during acidic reperfusion. However, on switching to pH 7.4, VF occurred in a further 50, 58, 0, and 0% of hearts, respectively; thus the overall incidences of VF were 67, 75, 42 (P < 0.05 vs. control), and 25% (P < 0.05 vs. control), respectively. Additional hearts (n = 8/group) were used for cytochemical determination of sarcolemmal Na(+)-K(+)-ATPase activity in both the ischemic/reperfused left ventricular (LV) and the nonischemic right ventricular (RV) free walls. Ischemia (10 min) reduced LV Na2(+)-K(+)-ATPase activity from 110 +/- 8 to 25 +/- 3% of the RV value. After 0.5, 1, 2, 3, and 4 min of acidic reperfusion, LV Na(+)-K(+)-ATPase activity was 24 +/- 3, 29 +/- 3, 37 +/- 5, 55 +/- 6, and 70 +/- 4, respectively (P < 0.05 vs. 10-min ischemia). No significant recovery of LV Na(+)-K(+)-ATPase activity occurred following up to 4 min of pH 7.4 reperfusion. In conclusion, 1) at least 2 min of acidic reperfusion is required to achieve sustained protection against VF and 2) the protective mechanism may involve enhanced recovery of Na(+)-K(+)-ATPase activity as well as inhibition of Na+ influx.

Na+/H+ exchange and reperfusion arrhythmias: protection by intracoronary infusion of a novel inhibitor.

Activation of sarcolemmal Na+/H+ exchange has been proposed as a causal factor in reperfusion arrhythmogenesis. To test this hypothesis, we determined the antiarrhythmic efficacy of two structurally distinct but equipotent Na+H+ exchange inhibitors, 5-(N-ethyl-N-isopropyl)amiloride (EIPA) and the novel drug, 3-methylsulfonyl-4-piperidinobenzoyl guanidine (HOE-694), in isolated rat hearts (n = 12/group) subjected to independent dual coronary perfusion. After 15 min of aerobic perfusion of both beds, flow to the left coronary bed (LCB) was terminated for 10 min; this was followed by 5 min of reperfusion. Various concentrations of each drug were selectively infused into the LCB either during the 5-min period preceding ischemia plus during reperfusion or during reperfusion alone. With the former protocol, 0.01, 0.1, 1, and 10 microM EIPA reduced the incidence of reperfusion-induced ventricular fibrillation (VF) from 92% in controls to 83, 83, 50, and 0% (P < 0.05); the number of hearts in sinus rhythm at the end of reperfusion was increased from 17 to 42, 25, 83 (P < 0.05), and 100% (P < 0.05). HOE-694, at the same concentrations, reduced VF incidence from 92% in control to 83, 58, 50, and 8% (P < 0.05); 25, 67, 75 (P < 0.05), and 100% (P < 0.05) of hearts were in sinus rhythm, compared with 17% of controls, at the end of reperfusion. Even when infused during reperfusion alone, both drugs afforded significant protection against reperfusion-induced VF, which did not differ significantly from that observed when the drugs were also given before ischemia. The similar antiarrhythmic efficacy of EIPA and HOE-694 is consistent with an arrhythmogenic role for activation of Na+/H+ exchange during early reperfusion.

Cardiodynamic and neurohormonal importance of atrial contribution in rate-responsive pacing.

To elucidate the physiologic importance of atrial contribution in recently developed rate-responsive pacing, changes in cardiodynamics and neurohormonal factors were analyzed during exercise in patients with respiratory rate-dependent, rate-responsive atrial (AAIR; n = 6) and ventricular (VVIR; n = 9) demand mode pacemakers implanted for sick sinus syndrome. With increasing pacing rate during bicycle ergometer exercise, the AAIR group had significant increases in cardiac index (p < 0.05), left ventricular ejection fraction (p < 0.05), and ejection (p < 0.05) and peak filling (p < 0.05) rates; however, the VVIR group had a significant decrease in ejection fraction (p < 0.05), and an increase in cardiac index (p < 0.05) that was significantly less than in the AAIR group. At rest, the mean plasma concentrations of atrial natriuretic peptide (p < 0.005) and cyclic guanosine monophosphate (p < 0.05) were significantly greater in the VVIR group than in the AAIR group and normal subjects (n = 8). Atrial natriuretic peptide, norepinephrine, and cyclic adenosine and guanosine monophosphates were significantly greater (p < 0.05) during exercise, and atrial natriuretic peptide was significantly greater in the VVIR group (207.5 +/- 8.3 pg/ml) than in the AAIR group (116.4 +/- 51.5) and normal subjects (30.8 +/- 19.2; p < 0.05); this suggested a further increase in the nonphysiologic atrial overload with VVIR pacing. The data show both the neurohormonal and cardiodynamic importance of atrioventricular synchrony in rate-responsive pacing.

Mechanisms of antifibrillatory effect of acidic reperfusion: role of perfusate bicarbonate concentration.

Transient (2 min) acidic (pH 6.6) reperfusion with low [HCO3-] solution suppresses reperfusion-induced ventricular fibrillation (VF) in the isolated rat heart. Using this preparation, we tested whether the effect was mediated by the high [H+] or the low [HCO3-] of perfusate. Left and right coronary beds were independently perfused with HCO3(-)-containing (25.0 mmol/l) solution at pH 7.4. Regional ischemia was then induced by stopping flow to the left coronary bed for 10 min. Hearts were subsequently assigned to four groups (n = 12 hearts/group), and the left coronary bed was reperfused with either HCO3(-)-containing (25.0 or 4.0 mmol/l) or HCO3(-)-free (5.0 mmol/l HEPES) solution, at pH 7.4 throughout (control reperfusion) or at pH 6.6 for the first 2 min and at pH 7.4 from 2 to 5 min (acidic reperfusion). Regardless of the buffer, controls exhibited a high (92 and 100%) incidence of VF; this was reduced to 42% in both of the acidic reperfusion groups (P < 0.05). There were no intergroup differences in heart rate, coronary flow, or size of ischemic zone. Thus high [H+], rather than low [HCO3-], appears to mediate the antifibrillatory effect of transient acidic reperfusion.

Reperfusion-induced arrhythmias. A role for washout of extracellular protons?

Rapid washout of extracellular H+ accumulated during preceding ischemia (i.e., the abrupt restoration of extracellular pH) has been implicated as an arrhythmogenic factor during reperfusion. Therefore, we hypothesized that by limiting the rate at which extracellular pH was restored during early reperfusion it should be possible to protect against reperfusion-induced arrhythmias. To test this, we used isolated rat hearts (n = 12 per group) and a novel dual coronary perfusion cannula that permitted the induction of regional ischemia (10 minutes) and the selective reperfusion (8 minutes) of the ischemic zone with modified solutions. We examined the antiarrhythmic efficacy of 1) acidic (pH 6.6) reperfusion with stepwise restoration of extracellular pH to 7.4 (stepped pH) and 2) transient (2-minute) acidic (pH 7.1, 6.8, 6.6, or 6.4) reperfusion with subsequent abrupt restoration of extracellular pH to 7.4. Hearts in two contemporary control groups were reperfused with solution at pH 7.4 throughout. In all groups, 100% of hearts exhibited ventricular tachycardia (VT) on reperfusion. VT degenerated into ventricular fibrillation (VF) in 100% of hearts in the control group but in only 42% of hearts in the stepped-pH group (p < 0.05). In the groups subjected to transient acidic reperfusion, there was a pH-dependent prolongation of VT cycle length (measured at 15 seconds of reperfusion), which was 47.1 +/- 3.9, 51.1 +/- 5.5, 56.0 +/- 1.9, 60.4 +/- 2.8 (p < 0.05), and 68.8 +/- 5.0 (p < 0.05) msec in the pH 7.4 (control), 7.1, 6.8, 6.6, and 6.4 groups, respectively. In these groups, VT degenerated into VF in 92%, 92%, 83%, 42% (p < 0.05), and 33% (p < 0.05) of hearts, respectively. In conclusion, limiting the rate at which extracellular pH is restored during early reperfusion does not affect the rapid induction of VT but inhibits the degeneration of VT into VF and promotes spontaneous reversion to normal sinus rhythm. This is consistent with a major arrhythmogenic role, during uncontrolled reperfusion, for the rapid washout of extracellular H+.

Rate of reflow and reperfusion induced arrhythmias: studies with dual coronary perfusion.

OBJECTIVE: The aim was to determine the relationship between the rate of reflow and vulnerability to reperfusion induced arrhythmias. METHODS: Isolated rat hearts, in which left and right coronary arteries were perfused independently, were subjected to transient (10 min) cessation of flow to the left coronary bed. During the subsequent 10 min of reperfusion, flow in the left coronary bed was regulated to create five different reflow profiles (n = 12 per group): (1) immediate restoration of 100% flow which was maintained throughout reperfusion (control); (2) stepwise restoration of flow with 10% flow from 0-1 min, 20% flow from 1-2 min, 40% flow from 2-3 min, 60% flow from 3-4 min, 80% flow from 4-5 min, and 100% flow from 5-10 min; (3) 10% flow from 0-5 min and 100% flow from 5-10 min; (4) 20% flow from 0-5 min and 100% flow from 5-10 min; and (5) 40% flow from 0-5 min and 100% flow from 5-10 min. RESULTS: There were no significant differences between the groups in the incidences of reperfusion induced ventricular tachycardia or fibrillation, which were 100% and 58-92%, respectively. However, the time to onset of reperfusion induced ventricular fibrillation was delayed (p less than 0.05) from 15 (SEM 1) s in group (1) to 191(39), 210(38), and 77(29) s in groups 2, 3, and 4, respectively. No significant delay was observed in group 5. There were no significant differences between the groups in size of ischaemic zone or heart rate. CONCLUSIONS: In crystalloid perfused hearts, restricted reflow delays the time to onset of reperfusion induced ventricular fibrillation but does not reduce the incidence of reperfusion induced ventricular tachycardia or fibrillation.

Disturbed secretion of atrial natriuretic peptide in patients with persistent atrial standstill: endocrinologic silence.

Persistent atrial standstill is a very rare pathophysiologic condition whose diagnosis is established when both electrical and mechanical silence of the atria are confirmed. To test the hypothesis that secretion of atrial natriuretic peptide is disturbed in patients with persistent atrial standstill, the response of atrial natriuretic peptide secretion and other neurohormonal factors during exercise was investigated in three patients with a rate-responsive ventricular demand (VVI) pacemaker implanted for confirmed persistent atrial standstill. The results were compared with those observed in eight normal subjects and patients with a rate-responsive VVI (Group A) or atrial demand (AAI) (Group B) pacemaker implanted for confirmed sick sinus syndrome. Patients in Group A displayed significant elevation of alpha-human atrial natriuretic peptide secretion both before and during exercise (122.5 +/- 14.8 and 207.5 +/- 8.3 pg/ml, respectively) compared with those in Group B (55 +/- 14.1 and 116.4 +/- 51.5 pg/ml, respectively) and the normal subjects (18.9 +/- 9.8 and 30.8 +/- 19.2 pg/ml, respectively). This indicated development of a nonphysiologic increase in atrial volume or pressure overload, or both, in rate-responsive VVI pacing because of lack of atrioventricular synchrony. However, patients with persistent atrial standstill had undetectable (less than 10 pg/ml) or almost undetectable secretion of atrial natriuretic peptide as well as lower levels of cyclic guanosine monophosphate in the circulation both before and during exercise. Changes in plasma catecholamines during exercise were similar in patients with persistent atrial standstill compared with the other groups. This study indicates that "endocrinologic silence" accompanies electrical and mechanical silence of the atria, which may constitute a third diagnostic clue to persistent atrial standstill.

[What plays an important role in the secretion of alpha-human atrial natriuretic polypeptide (alpha-hANP) during the early stage of acute myocardial infarction?].

To clarify the factors stimulating the secretion of alpha-human atrial natriuretic polypeptide (alpha-hANP) during the early stage of acute myocardial infarction (AMI), the plasma alpha-hANP level was sequentially measured and evaluated in terms of correlation with the severity of AMI, cardiovascular hemodynamics and endocrine functions in 61 patients with AMI. The plasma alpha-hANP levels within 24 hrs, from 48 to 72 hrs, and from 120 to 168 hrs after the onset of AMI were 213.8 +/- 198.0, 152.0 +/- 131.2, and 156.0 +/- 166.4 pg/ml, respectively, all of which were significantly higher compared to the control level (29.6 +/- 9.3 pg/ml). In surviving patients, the level of plasma alpha-hANP within 24 hrs was significantly higher than those in 48-72 and 120-168 hrs. On the contrary, non-surviving patients displayed prolonged elevation of alpha-hANP during the early stage of AMI. The initial alpha-hANP levels in Killip I, II, III and IV patients were 229.3 +/- 232.7 (n = 43), 216.7 +/- 86.6 (n = 7), 243.3 +/- 113.5 (n = 6) and 282.0 +/- 224.6 pg/ml (n = 5), respectively, and there were no significant differences between the categories.(ABSTRACT TRUNCATED AT 250 WORDS)