Evaluation of antihypertensive effects of once-a-day isradipine and fosinopril: A double-blind crossover study by means of ambulatory blood pressure monitoring

We compared the efficacy and tolerability of is-radipine (ISR) and fosinopril (FOS) once-a-day administration in 17 outpatients, 9 men and 8 women, aged 35–65 years (mean ± SD= 58 ± 10 years), affected by mild to moderate primary systemic hypertension. The patients were given single-blind placebo for 2 weeks and thereafter, in double-blind, randomized, crossover sequence, ISR (5 mg) and FOS (20 mg), both for 4 weeks. At the end of each period, patients underwent 24-h noninvasive blood pressure (BP) monitoring by means of an A&D TM 2420 Monitor Model 7, with readings taken every 10 min during the day (from 7 A.M. to 11 P.M.), and every 20 min during the night (from 11 P.M. to 7 A.M.). Similarly, BP load (BPL) as percentage of systolic and diastolic BP reading > 140 and > 90 mmHg was investigated. Both ISR and FOS induced a highly significant (p<0.0001) decrease in BP from 158/96 ± 7/6 mmHg to 133/86 ± 6/6 and to 132/83 ± 10/7 mmHg, respectively. Mean BP decreased from 117 ± 6 mmHg to 102 ± 6 mmHg (ISR) (p<0.0001) and to 99 ± 8 mmHg (FOS) (p<0.0001). Both ISR and FOS significantly (p<0.0001) reduced systolic BPL from 78 ± 16% to 44 ± 13% and 28 ± 12%, respectively, and diastolic BPL from 70 ± 15% to 40 ± 13% (p<0.0001) and 35 ± 13% (p<0.0001), respectively. A significant difference between the two drugs in systolic (p<0.0002) BPL was observed. No significant differences in heart rate were noted. No unexpected adverse effects were observed in any patient under either therapy. Both ISR and FOS resulted in very effective decrease in BP; however, FOS proved to be significantly more effective than ISR.     

Impact of pharmacy outreach services on blood pressure management in the elderly community of Hong Kong

Aim: To investigate the impact of the Pharmacy Outreach Service (POS) on blood pressure (BP) and disease knowledge among community‐dwelling elderly patients with hypertension, and to evaluate the sustainability of such impact of POS. Methods: A prospective open‐labeled study of elderly adults (aged ≥65 years) with hypertension (BP ≥140/90 mmHg for non‐diabetics and ≥130/80 mmHg for diabetics) was carried out at seven elderly community centers from July 2008 to March 2010. Pharmacists provided BP monitoring, medication review and disease knowledge assessment. The target BP was <140/90 mmHg for non‐diabetics and <130/80 mmHg for diabetics. The primary outcome was BP change, whereas the secondary outcome was the change of disease knowledge of hypertension. All outcomes were compared between baseline and the last visit. For POS 2008/09 participants, BP was compared between values obtained during POS 2008/09 and 2009/10. Results: A total of 97 participants were recruited. Systolic BP reduced significantly from 152.38 ± 18.80 mmHg to 147.04 ± 20.72 mmHg (P = 0.021), and diastolic BP reduced from 73.84 ± 11.36 mmHg to 71.03 ± 10.97 mmHg (P = 0.010). Cumulative reductions in mean systolic BP and diastolic BP throughout the 2‐year study period were 21.39 ± 24.72 mmHg and 9.88 ± 13.48 mmHg, respectively (P < 0.001). A 12% increase in the at‐goal rate was observed in new participants recruited in 2009 (P = 0.039). Disease knowledge of hypertension improved significantly (P < 0.005), particularly in areas that included the definition of hypertension, diet and lifestyle modification. Conclusions: The POS might improve blood pressure control, hypertension and diabetes knowledge in elderly adults with hypertension in Hong Kong. The effect on blood pressure improvement was sustainable. Geriatr Gerontol Int 2013; 13: 175–181.     

Preferred QT Correction Formula for the Assessment of Drug‐Induced QT Interval Prolongation

Drug‐Induced QTc Interval Assessment. Introduction: There is debate on the optimal QT correction method to determine the degree of the drug‐induced QT interval prolongation in relation to heart rate (ΔQTc). Methods: Forty‐one patients (71 ± 10 years) without significant heart disease who had baseline normal QT interval with narrow QRS complexes and had been implanted with dual‐chamber pacemakers were subsequently started on antiarrhythmic drug therapy. The QTc formulas of Bazett, Fridericia, Framingham, Hodges, and Nomogram were applied to assess the effect of heart rate (baseline, atrial pacing at 60 beats/min, 80 beats/min, and 100 beats/min) on the derived ΔQTc (QTc before and during antiarrhythmic therapy). Results: Drug treatment reduced the heart rate (P < 0.001) and increased the QT interval (P < 0.001). The heart rate increase shortened the QT interval (P < 0.001) and prolonged the QTc interval (P < 0.001) by the use of all correction formulas before and during antiarrhythmic therapy. All formulas gave at 60 beats/min similar ΔQTc of 43 ± 28 ms. At heart rates slower than 60 beats/min, the Bazett and Framingham methods provided the most underestimated ΔQTc values (14 ± 32 ms and 18 ± 34 ms, respectively). At heart rates faster than 60 beats/min, the Bazett and Fridericia methods yielded the most overestimated ΔQTc values, whereas the other 3 formulas gave similar ΔQTc increases of 32 ± 28 ms. Conclusions: Bazett's formula should be avoided to assess ΔQTc at heart rates distant from 60 beats/min. The Hodges formula followed by the Nomogram method seem most appropriate in assessing ΔQTc. (J Cardiovasc Electrophysiol, Vol. 21, pp. 905‐913, August 2010)     

Twenty-four-hour blood pressure monitoring and effects of indapamide

Twenty-four-hour blood pressure (BP) monitoring with a noninvasive device (Kontron) has been used to assess the effect of a single dose of indapamide in a group of patients with essential hypertension. Originally 23 patients were selected. Three patients withdrew from the study because of refusal to go through the second 24-hour recording. Eight of the remaining patients had to be excluded for technical reasons, which left 12 patients available for analysis. All patients received a single dose of indapamide, 2.5 mg/day. Before treatment began, a 24-hour BP control was performed, and a second one a month later (37 +/- 8 days). The age of the patients was 46 +/- 10 years. Diurnal BP (8 am to 10 pm) and heart rate were, respectively, 148 +/- 15/101 +/- 6 mmHg and 79 +/- 9 beats/min; night BP (10 pm to 8 am) was 131 +/- 15/88 +/- 7 mmHg and heart rate 71 +/- 10 beats/min. After therapy, diurnal BP was 131 +/- 15/92 +/- 7 mmHg (-15 +/- 7/-8 +/- 4: p less than 0.0001/p less than 0.0001); heart rate 82 +/- 8 beats/min (difference not significant); night BP was 115 +/- 13/80 +/- 8 mmHg (-16 +/- 11/-8 +/- 7: p less than 0.0001/p less than 0.0001) and heart rate 70 +/- 9 beats/min (difference not significant). Twenty-four-hour systolic work values were 106 +/- 15 at the beginning of the trial and 96 +/- 14 (-9.7 +/- 14; p less than 0.05) after 1 month of indapamide treatment. Variability did not change with treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute increase in right atrial pressure by intracardiac stimulation releases atrial natriuretic peptide

We studied the effect of an increase in heart rate and/or inright atrial pressure (RAP) on the release of at rial natriureticpeptide (ANP) in 18 patients. In group 1 (n = 6), right ventricularstimulation (100, 120, 140 and 150 bpm) was used to increaseRA P by asynchronous contraction of the right atrium and ventricle.Mean RA P increased from 3.9 ±0.2 to 8.3±0–6mmHg(mean±SEM). Median ANP levels increased from 120 to 440pgml^–1(P<0.05). In group 2 (n = 6), right atrial stimulation below140 bpm did not have any effect on ANP or RAP, but at a rateabove 140 bpm RAP increased from 5.8 ± 0.5 to 7.5 ±0.5mmHg and ANP from 226 to 396 pg ml^–1 (P < 0.05). Ingroup 3 (n - 6), RA P or ANP were not influenced by continuousright atrial stimulation at 110 bpm. Plasma cyclic GMP levelsparalleled the changes in plasma ANP. Thus, an acute incrementof RAP results in a release of ANP, but acceleration of heartrate alone has no effect on ANP secretion.     

Comparison of dopamine and dobutamine in patients requiring postoperative circulatory support

We compared dopamine and dobutamine following cardiac surgery in a sequential cross-over study of 9 patients who required inotropic support after volume replenishment. Seven patients had mitral valve replacement, 2 with simultaneous coronary revascularization (CABG), and 1 each with simultaneous tricuspid annuloplasty and aortic valve replacement; 1 had isolated CABG and 1 had repair of a postinfarction ventricular septal defect. Heart rate, right and left atrial pressures, pulmonary and mean arterial pressure, systemic and pulmonary vascular resistance, and cardiac index were measured and calculated. Inotropic support with dopamine or dobutamine was begun for treatment of low cardiac index within 12 hours postoperatively. Measurements were made after 20 minutes on either agent at 5–10 m?g/kg per min when cardiac output and general clinical state were stable. Each patient was then switched to the other agent at approximately the same dose rate, titrating the dosage to the same cardiac output, and repeat measurements were made at 20 minutes when again stable. Similar dosages of dopamine (6.2±1.7 m?g/kg/min) and dobutamine (6.7±2.5 m?g/kg/min) produced equivalent heart rate (103±19 vs. 102±13 beats/min, p=NS), cardiac index (2.8±1.1 vs. 2.9±1.2 l/min/m², p=NS), and pulmonary arterial pressure and vascular resistance. Mean systemic arterial pressure was significantly lower with dobutamine (59±5 vs. 67±7 mmHg, p<0.05) as were mean left (14±5 vs. 18±6 mmHg, p<0.0001) and right (9±2 vs. 11±2 mmHg, p<0.05) atrial pressures. Systemic vascular resistance was also reduced with dobutamine but the difference was not statistically significant.     

Response of normal and abnormal sinus node to right ventricular stimulation

Right ventricular pacing at progressively increasing rates was performed in 25 patients with complete ventriculoatrial block, before and after autonomic blockade with intravenous propranolol and atropine. At the end of each ventricular pacing stage a right intraatrial electrogram and electrocardiographic leads were simultaneously recorded. The relation between right ventricular pacing and atrlal rates was studied from the recordings obtained at each pacing stage in both group I,8 patients with sick sinus syndrome, and group II, 17 patients with normal sinus function. Right ventricular pacing was associated with an increment in atrial rate that was significantly smaller (probability [p]<0.001) in patients In group I (mean ± standard error of the mean 8 ± 6 beats/mln) than in group II (mean 25 ± 10 beats/min). The maximal atrial rate reached during right ventricular pacing exceeded 80 beats/min in all patients In group II but remained less than 74 beats/min in patients in group I. Because autonomic blockade did not significantly Influence the preceding results, it is concluded that a mechanical effect on the sinus node may explain this phenomenon.     

Correction for Heart Rate Is Not Necessary for QT Dispersion in Individuals without Structural Heart Disease and Patients with Ventricular Tachycardia

Background: It remains controversial whether QT dispersion should be corrected for heart rate, especially when the limitations of rate correction formulae are considered. We investigated whether incremental atrial pacing affects QT dispersion and the rate‐corrected values according to Bazett's formula in individuals without structural heart disease and in patients with history of sustained ventricular tachycardia. Methods: We studied 32 individuals without structural heart disease (group A), and 16 patients with a history of sustained ventricular tachycardia (group B). QT dispersion and corrected for heart rate QT dispersion using Bazett's formula (QTc dispersion) were calculated in sinus rhythm, and during continuous right atrial pacing for one minute at 100 and 120 beats/min. Results: Interobserver variability was not significant (P ≧ 0.10). QT dispersion did not differ at rest between groups A and B and did not change significantly from baseline at any heart rate in both groups. However, QTc dispersion increased significantly with atrial pacing in a similar manner in group A and group B (42 ± 19 ms at rest vs 53 ± 23 ms at 120 beats/min, P < 0.001 for group A, 39 ± 16 ms at rest vs 60 ± 19 ms at 120 beats/min, P < 0.001 for group B). Conclusions: We conclude that QT dispersion remains unchanged during atrial pacing at heart rates up to 120 beats/min in both individuals without structural heart disease and in patients with a history of sustained ventricular tachycardia. Correction by Bazett's formula results in prolongation of QTc dispersion, yielding values which may be misleading. A.N.E. 2002;7(1):47–52     

Effects of daily walking on office,home and 24-h blood pressure in hypertensive patients

Abstract

Aerobic exercise has been recommended in the management of hypertension. However, few studies have examined the effect of walking on ambulatory blood pressure (BP), and no studies have employed home BP monitoring. We investigated the effects of daily walking on office, home, and 24-h ambulatory BP in hypertensive patients. Sixty-five treated or untreated patients with essential hypertension (39 women and 26 men, 60?±?9 years) were examined in a randomized cross-over design. The patients were asked to take a daily walk of 30–60?min to achieve 10?000 steps/d for 4 weeks, and to maintain usual activities for another 4 weeks. The number of steps taken and home BP were recorded everyday. Measurement of office and ambulatory BP, and sampling of blood and urine were performed at the end of each period. The average number of steps were 5349?±?2267/d and 10?049?±?3403/d in the control and walking period, respectively. Body weight and urinary sodium excretion did not change. Office, home, and 24-h BP in the walking period were lower compared to the control period by 2.6?±?9.4/1.3?±?4.9?mmHg (p?<?0.05), 1.6?±?6.8/1.5?±?3.7?mmHg (p?<?0.01), and 2.4?±?7.6/1.8?±?5.3?mmHg (p?<?0.01), respectively. Average 24-h heart rate and serum triglyceride also decreased significantly. The changes in 24-h BP with walking significantly correlated with the average 24-h BP in the control period. In conclusion, daily walking lowered office, home, and 24-h BP, and improved 24-h heart rate and lipid metabolism in hypertensive patients. However, the small changes in BP may limit the value of walking as a non-pharmacologic therapy for hypertension.     

Value of conventional and tissue Doppler echocardiography in the noninvasive measurement of right atrial pressure

Background: Evaluation of right atrial pressure (RAP) provides useful diagnostic, therapeutic, and prognostic information. Aim: To assess the utility of several conventional and tissue Doppler parameters in the estimation of RAP. Methods: Among 50 consecutive patients (median age: 50 years; all in sinus rhythm), invasively measured RAP was simultaneously correlated with pulsed Doppler of tricuspid inflow (peak E and A velocities, E‐wave deceleration time) and pulsed tissue Doppler of lateral tricuspid annulus (peak E’ and A’ velocities, isovolumic relaxation time [IVRT], acceleration time and rate of E’‐wave, deceleration time and rate of E’‐wave). These ratios were calculated: E/A, E’/A’, E/E’, and E/IVRT. Results: The median RAP was 14 mmHg (range 1–27 mmHg) with 29 patients (58%) having an elevated RAP (>10 mmHg). Among all studied Doppler variables, E/E’ ratio showed the strongest correlation with RAP (r = 0.84, P < 0.001) with the following regression equations: RAP = 1.24 + (1.69 × E/E’). The mean difference between Doppler and invasively measured RAP was 0.21 ± 2.6 mmHg. E/ E’ ratio ≥ 4.5 provides 89% sensitivity and 100% specificity for detection of elevated RAP (receiver operating characteristic area 0.95; P < 0.001). Conclusion: Of all echocardiographic variables investigated, tricuspid annular E/E’ ratio is identified as the best index for noninvasive determination of RAP.     

Reversibility of hypotension and shock by atrial or atrioventricular sequential pacing in patients with right ventricular infarction

Hypotension and shock associated with heart block and other forms of atrioventricular (AV) dissociation frequently accompany right ventricular infarction (RVI). Such patients do not invariably improve with ventricular pacing. We evaluated the relative effects of AV dissociated rhythms (ventricular pacing or nodal rhythm) and AV synchronous rhythms (atrial pacing, AV sequential pacing, or return to normal sinus rhythm) in seven patients with RVI complicated by AV dissociation, who had hypotension or shock. Hemodynamic monitoring demonstrated the characteristic features of RVI in all patients. Restoration of AV synchrony resulted in a highly significant (p ≤ 0.001) increase in systolic blood pressure (88.0 ± 16.5 mm Hg to 133.0 ± 21.8 mm Hg), cardiac output (3.8 ± 0.9 L/min to 5.7 ± 0.9 L/min), and stroke volume (40.5 ± 6.9 cc to 61.0 ± 10.0 cc). We conclude that restoration of normal AV synchrony has a marked effect on stroke volume in this setting and that atrial or AV pacing can reverse hypotension and shock in RVI complicated by AV dissociation.     

Evidence for transient limitations in coronary blood flow during unstable angina pectoris: hemodynamic changes with spontaneous pain at rest versus exercise-induced ischemia following stabilization of angina

The pathophysiologic basis for the deterioration of patients with stable angina pectoris to unstable angina is unclear. Central to this issue is the question of whether myocardial ischemia occurs at the same or at a lower myocardial oxygen demand during unstable periods as during stable periods. Consequently, we compared myocardial oxygen demand in 12 patients at the onset of spontaneous pain during unstable angina to myocardial oxygen demand during exercise-induced ischemia after resumption of stable angina, 6–12 weeks later. Myocardial oxygen demand was estimated from values for heart rate (HR), systolic blood pressure (BP), and the rate-pressure product (RPP). Rate-pressure product is the heart rate × systolic blood pressure × 10^-2 (mmHg/min/10²). There was definite evidence for coronary artery spasm for only one patient. There was no difference in heart rate, blood pressure, or rate-pressure product during pain-free intervals in the hospital and just before the start of exercise testing. Mean H R (71.2± 11.1 beats/min; mean ± standard deviation) and RPP (95.8±20.0 mmHg/min/10²) just before spontaneous angina during the unstable period were significantly lower (p<0.001) than at the termination of bicycle ergometry in both the supine (HR, 96.9±10.5 beats/min; RPP, 141.8±25.0 mmHg/min/10²) and upright (HR, 98.1±13.6 beats/min; RPP, 143.0±32.2 mmHg/min/10²) positions. Blood pressure (134.5 ± 17.6 mmHg) just before spontaneous angina was significantly lower than at the conclusion of both supine (145.6±13.3 mmHg) and upright (145.1 ±18.6 mmHg) ergometry. The observation that myocardial oxygen demand was lower at the threshold of ischemia with spontaneous angina than with exercise-induced ischemia is consistent with the hypothesis that there were transient, reversible limitations in coronary blood flow during the period of unstable angina. There was also a moderate but significant rise in estimated myocardial oxygen demand just before spontaneous angina in these patients, but the nature of the data do not allow us to distinguish whether or not this rise was part of the cause or an effect of ischemia. While the results of this study did not identify the cause for the transient limitations in coronary flow, coronary artery spasm without ST-segment elevation, intracoronary platelet aggregates, and hemorrhage into atherosclerotic plaques are possibilities that are consistent with these hemodynamic observations.     

Routine arterial oxygen saturation monitoring is not necessary during transesophageal echocardiography

Background: Transesophageal echocardiography (TEE) is now an established adjunct to routine echocardiography, its diagnostic impact making it an invaluable first-line diagnostic procedure in many cardiac conditions. However, there is no unanimity in the way the transesophageal procedure is carried out, especially with regard to the need for antibiotic prophylaxis, sedation, and the monitoring of oxygen saturation. Hypothesis: This study was prospectively undertaken (1) to determine the presence and magnitude of oxygen desaturation and (2) the changes in heart rate and blood pressure following sedation for routine TEE in an unselected and consecutive group of patients to identify those at high risk. Methods: Arterial oxygen saturation, heart rate, and systolic, diastolic, and mean blood pressure were monitored in 106 consecutive patients undergoing routine transesophageal echocardiography. Ninety-four (89%) patients received intravenous sedation with midazolam. Results: Three min after midazolam administration there was a drop in oxygen saturation from 97 ± 2.5 to 95 ± 2.9 (p<0.001), in systolic blood pressure from 139 ± 19.5 to 124.8 ± 22.2 mmHg (p<0.001), in diastolic blood pressure from 86.6 ± 19.9 to 77.5 ± 17.7 mmHg (p<0.001), and in mean blood pressure from 108.3 ± 18 to 95.6 ± 28.8 mmHg (p<0.001). After introduction of the transesophageal probe and during the examination, there was a further drop in oxygen saturation with a maximum drop at the 15th min of the examination (93.7 ± 3.7 vs. 97 ± 2.5, p<0.001). The maximum blood pressure drop occurred at the 12th min into recovery: systolic blood pressure dropped from 139 ± 19.5 to 118 ± 20.8 mmHg (p<0.001), diastolic blood pressure from 86.6 ± 16.9 to 75.8 ± 17.9 mmHg (p<0.005), and mean blood pressure from 108.3 ± 18 to 92.5 ± 19.4 mmHg (p<0.01). Patients with congestive heart failure had a greater drop in oxygen saturation compared with patients who were not in heart failure (p<0.01). Twelve patients did not receive any sedation; however, they all showed a drop in oxygen saturation from 97.8 ± 2.3 to 94.6 ± 3.4 (p<0.001), with a maximum drop at the 15th min during the transesophageal examination. Conclusion: In patients with no chronic obstructive airway disease who are not in congestive heart failure, routine oxygen saturation monitoring is not deemed necessary during transesophageal examination. The cause of hypoxemia during the procedure is not only related to sedation but also to esophageal intubation.     

Contraction-excitation feedback in human atrial fibrillation

Background: Contraction-excitation feedback, that is, electrophysiologic changes that are caused or preceded by mechanical changes of the myocardium, has been extensively studied in the ventricles. The role of contraction-excitation feedback in the atria, and more particularly in the genesis and maintenance of atrial fibrillation, has been less adequately investigated. Hypothesis: The aim of the present study was to determine whether increased right atrial pressure (RAP) facilitates the induction of atrial fibrillation (AF) in patients with a history of lone AF. Methods: Sixteen patients with a history of paroxysmal AF but without structural heart disease were included in the study. All patients underwent electrophysiologic study at both a lower (3.1 ± 2.0 mmHg) and (in 13 cases) a higher (6.4 ± 2.5 mmHg) RAP. “Higher” was considered the pressure following rapid (in about 30 min) intravenous administration of normal saline or before the administration of a diuretic. Results: Rapid atrial pacing induced AF in 19 of 29 attempts. At a lower pressure, rapid pacing induced brief (3 s to 3 min) AF in 3 of 16 patients, long-lasting (>3 min) AF in 3 of 16 patients, and no AF in 10 of 16 patients. At a higher pressure, brief AF was induced in 3 of 10 patients in whom no AF could be induced at a lower pressure, and long-lasting AF in 10 patients in whom either brief AF (3 cases) or no AF (7 cases) was induced at a lower pressure. In 11 patients, in whom Wenckebach periodicity was determined at both higher and lower pressure, the critical cycle length at which atrioventricular block appeared was significantly (p<0.001, paired t-est) longer(349.1 ± 44.4 ms, i.e.,+15.5 ± 11.3 ms)at higher than at lower atrial pressure (333.6 ±41.0 ms). In nine patients, in whom Wenckebach periodicity was determined and two rhythms occurred at different pressures, the critical cycle length was 332.2 ± 45.8 ms when associated with sinus rhythm, and significantly (p<0.01) longer (344.4 ± 48.0 ms, i.e., +12.2 ± 8.3 ms) when associated with induction of AF. Conclusion: In patients with lone atrial fibrillation, modest increases in atrial pressure may facilitate the induction of atrial fibrillation.     

Beta-blockers in hypertensive non-insulin-dependent diabetics: Comparison between penbutolol and propranolol on metabolic control and response to insulin-induced hypoglycemia

Summary In a single blind randomized study the effects of a 4-week administration of propranolol (160 mg/day) and penbutolol (40 mg/day) on metabolic control and insulin-induced hypoglycemia were tested in 8 non-insulin-dependent diabetics with diastolic blood pressure between 95 and 110 mmHg. The recovery from hypoglycemia was not delayed by either drug; hypoglycemic nadir and Conard’sK did not change significantly. Symptoms of hypoglycemia were inhibited to a lesser extent and pulse rate decrease was lower after penbutololvs baseline (65±2.4vs 77±2.4 beats/min, p<0.01) than after propranololvs baseline (61±1.06vs 77±2.4 beats/min p<0.001). Both drugs produced similar and significant effects on blood pressure both systolic and diastolic. There were no significant effects on fasting plasma glucose concentration, HbA_tc, IRI, urinary C-peptide, triglycerides, total and HDL cholesterol and FFA. IRG decreased after penbutololvs baseline 60 min after insulin injection (170±30.8vs 125±15.4 pmol/l, p<0.05). These results indicate that the use of beta-blockers, in particular penbutolol, for mild to moderate hypertension may be considered the treatment of choice also in non-insulin-dependent diabetics at the therapeutic doses employed.     

The effect of Mid-Day Sleep on blood pressure levels in patients with arterial hypertension

Study objectivesLifestyle changes decrease blood pressure (BP) levels by 3-5 mmHg in hypertensive patients. We assessed the effect of mid-day sleep on BP levels in hypertensive patients.MethodsWe prospectively studied two hundred and twelve hypertensive patients. Mid-day sleep duration, lifestyle habits, anthropometric characteristics, office BP, ambulatory BP monitoring, pulse wave velocity (PWV), augmentation index (AI) were recorded. A standard echocardiographic evaluation was performed.Results53.8% were females, mean age was 62.5±11.0 years and mean body mass index was 28.9±5.4kg/m². Mean average 24h systolic and diastolic BP (SBP & DBP) was 129.9±13.2/76.7±7.9 mmHg respectively. The majority was non-smokers (70.3%) and did not have diabetes (74.7%). The mean midday sleep duration was 48.7±54.3 min. Average 24h SBP (127.6±12.9 mmHg vs 132.9±13.1 mmHg), average daytime SBP & DBP were lower in patients who sleep at midday, compared to those who do not (128.7±13/76.2±11.5 vs 134.5±13.4/79.5±10.4 mmHg) (p<0.005). The effect was not correlated to the dipping status. Midday sleep duration was negatively correlated with average 24h SBP & daytime SBP. In a linear regression model, for every 60 min of midday sleep, 24h average SBP decreases by 3 mmHg (p<0.001). There were no differences in the number of antihypertensive medications, PWV, AI or echocardiographic indices between study groups.ConclusionsMid-day sleep significantly decreases average 24h and daytime SBP/DBP in hypertensives. Its effect seems to be as potent as other well-established lifestyle changes and is independent of dipping status.     

Caloric restriction alters arterial blood pressure and baroreflex responsiveness of the spontaneously hypertensive rat

Aging is associated with an increase in blood pressure and the occurrence of hypertension. Caloric restriction retards the aging process, in general, and is a commonly used therapeutic approach to the control of high blood pressure. The aim of this study was to examine the effects of long term caloric restriction on mean arterial blood pressure, heart rate and the baroreflex responsiveness of spontaneously hypertensive (SH) rats. Male, 3-month-old SH rats were allowed to eat ad libitum or were fed only 60% of the ad libitum amount. After 4 months, cannulas were inserted in the left femoral artery and vein under anesthesia. On the following day the blood pressure and heart rate were measured in the conscious rat. The basal mean arterial pressure of the calorie restricted rats (166±4 mm Hg, N=5) was significantly less than that of the ad libitum fed rats (182±4 mm Hg, N=4). The basal heart rates of the calorie restricted and ad libitum fed rats were 296±12 beats/min and 323±8 beats/min, respectively. The difference between the means was not significant (p>0.1). Nitroprusside and phenylephrine infusions were used to induce hypotensive and hypertensive episodes, respectively. For nitroprusside, the relationship between the change in mean arterial pressure and the reflex heart rate response was significantly steeper in the calorie restricted group (1.90±0.37 beats/min/mm Hg) than in the ad libitum fed group (0.86±0.1 beats/min/mm Hg). For phenylephrine the relationships were 0.98±0.09 and 0.52±0.18 beats/min/mm Hg, respectively. These results demonstrate that chronic caloric restriction reduces mean arterial pressure and enhances baroreflex responsiveness in the SH rat.     

Blood pressure and autonomic responses following isolated and combined aerobic and resistance exercise in hypertensive older women

Purpose: This study aimed to compare blood pressure (BP) after isolated and combined sessions of aerobic and resistance exercises in hypertensive older women. Heart rate (HR) and heart rate variability (HRV) were included as additional variables. Methods: Twenty-one older women (63±1.9 years; 69.9±2.7 kg; 158.8±2.1 cm) with controlled hypertension (resting BP = 132.2 ± 3.1/74.1 ± 4.0 mmHg) performed four random sessions on different days: 1) aerobic exercise (AE: treadmill walking/running; 40 min; 50–60% HR_reserve); 2) resistance exercise (RE: 8 exercises; 3 sets; 15 reps; 40% 1RM)); 3) aerobic exercise followed by resistance exercise (A+R); 4); control (CON). BP, HR and HRV were measured at rest and during 180 min after the sessions. Results: The AE and A+R sessions demonstrated significant decreases in SBP and DBP (30, 60, 120, and 180 min; P < 0.05) and increases in HR (30 and 60 min; P < 0.05) compared to the CON. The RE session demonstrated significant reductions compared to the CON only for DBP (120 and 180 min; P < 0.05). No significant differences were observed in HRV between resting and all sessions. Conclusion: All sessions that involved aerobic exercise (AE and A+R) caused postexercise hypotension in comparison to the CON, with no differences in HRV.     

Acute hemodynamic deterioration during rapid atrial pacing in patients with hypertrophic cardiomyopathy

Background and hypothesis: Supraventricular tachycardia and ventricular tachycardia are often observed in patients with hypertrophic cardiomyopathy (HCM) and they often alter the clinical features of HCM. We examine the influence of supra-ventricular tachycardia on cardiac function and assess the clinical characteristics of patients with HCM. Methods: We studied 32 patients with HCM and 8 normal volunteers using echocardiography under transesophageal rapid atrial pacing. Results: Presyncope-associated hypotension was observed during rapid atrial pacing in 8 HCM patients, but in none of the normal controls. During rapid atrial pacing (144 ± 8 beats/min in HCM, 146 ± 5 beats/min in controls), systolic blood pressure (SBP), the product of left ventricular filling volume (FV) and heart rate, and fractional shortening (%FS) in the HCM patients decreased significantly compared with the basal values (138 ± 19 mmHg vs. 99 ± 24 mmHg, 5.0 ± 1.21/min vs. 2.9 ± 0.91/min, 41.7 ± 6.2 % vs. 35.2 ± 6.0%, respectively), but these decreases were not observed in normal controls. The decrement of SBP during rapid atrial pacing in HCM patients with a history of syncope was more marked than that in those without such history. The decrement correlated positively with the indices of left ventricular hypertrophy (maximal wall thickness and wall thickness index) and with %FS, and correlated negatively with the endsystolic left ventricular diameter at rest. Conclusions: In some patients with HCM, supraventricular tachycardia causes marked hemodynamic deterioration that may be related to a history of syncope, marked hypertrophy, hyperkinesis, small cavity size, and small filling volume of the left ventricle.     

Influence of heart rate on systolic time intervals: Effects of atrial pacing versus dynamic exercise

The effects of atrial pacing and dynamic exercise in the supine position on systolic time intervals (STI) were compared in 10 normals. In another group of 13 normals, the effect of exercise alone on STI was tested. A linear shortening of electromechanical systole (QS₂) and left ventricular ejection time (LVET) with increasing heart rate was demonstrated with right atrial pacing and dynamic exercise in the frequency range between 60 and 140 beats/min. However, the shortening of LVET was significantly less (p<0.01) with exercise compared to pacing. This is explained by an increase in left ventricular stroke volume with exercise. The pre-ejection period (PEP) was significantly (p<0.001) shortened with exercise, but there was no change with atrial pacing. Thus, changes in heart rate (HR) alone, without changes in the dynamic state of the heart, did not influence PEP. It is suggested that PEP at rest should not be corrected for heart rate. The supine exercise regression equations for correction of heart rate for LVET and PEP differ from both the resting and the upright exercise regression equations. With exercise a frequency correction of STI using regression equations should be abandoned. Instead, uncorrected STI at standard heart rates (e.g., 100, 110, and 130 beats/min) should be taken for comparison. Heart rate standardization should be employed using the formula