Peak Exercise Systolic Blood Pressure Research Articles

Metabolic syndrome and exaggerated blood pressure response to exercise in newly diagnosed hypertensive patients

Running evidence supports a prognostic value of an exaggerated blood pressure response to exercise (EBPR). The impact of the metabolic syndrome (MS) on EBPR in hypertensive patients has not been investigated. A cross-sectional study in the setting of an outpatient hypertension clinic. In total, 325 non-diabetic patients with newly diagnosed hypertension were divided into two groups based on the presence (n = 95) or absence (n = 230) of the MS as defined with NCEP-ATP III criteria. All subjects underwent ambulatory blood pressure monitoring, echocardiography and exercise treadmill testing. Hypertensive patients with MS exhibited higher prevalence of EBPR (by 17%, p = 0.002) and peak exercise systolic BP (by 10.4 mmHg, p = 0.001) irrespectively of confounders. Metabolic equivalents were higher in hypertensives with MS (by 0.6 ml/kg/min, p = 0.048), but the difference lost significance after adjusting for confounders, including body mass index. Logistic regression analysis identified the MS as an independent predictor of an EBPR (p = 0.016). Hypertensive patients with MS had a 2.3-fold risk of exhibiting EBPR compared to those without MS. However, individual components of MS altogether as well as each one separately failed to predict EBPR. Presence of MS in newly diagnosed hypertensive patients is associated with increased peak exercise BP and a higher frequency of EBPR over and above its separate elements.

Usefulness of Exercise-Induced Hypertension as Predictor of Chronic Hypertension in Adults After Operative Therapy for Aortic Isthmic Coarctation in Childhood

Chronic hypertension is a major concern in adults who have undergone resection of coarctation of the aorta (CoA) in childhood. In otherwise healthy subjects, exercise-induced hypertension is prognostic for chronic hypertension; however, the prognostic value in patients with CoA remains unknown. The aim of the present study was to evaluate the predictive value of exercise-induced hypertension for chronic hypertension in these patients. In the present prospective follow-up study, 74 patients with CoA (58% men, age 30.9 ± 9.5 years) underwent ambulatory blood pressure (BP) monitoring and exercise testing twice from 2001 to 2009 with a follow-up period of 6.3 ± 0.8 years. Hypertension was defined as a mean systolic BP ≥140 mm Hg and/or mean diastolic BP ≥90 mm Hg or the need for antihypertensive treatment. Exercise-induced hypertension was defined as a mean systolic BP of <140 mm Hg and peak exercise systolic BP of ≥200 mm Hg. At baseline, 27 patients (36%) were hypertensive, 11 (15%) had exercise-induced hypertension, and 36 (49%) were normotensive. At follow-up, all 27 hypertensive patients remained hypertensive. Of the 11 with exercise-induced hypertension, 7 (64%) had developed chronic hypertension, and 4 (36%) continued to have exercise-induced hypertension. Of the 36 normotensive patients, 7 (19%) had developed hypertension, 12 (33%) had developed exercise-induced hypertension, and 17 (47%) remained normotensive. On multivariate analysis, baseline maximum exercise systolic BP was independently associated with the mean systolic BP at follow-up (β = 0.13, p = 0.005). In conclusion, the maximum exercise systolic BP was a predictor for chronic hypertension in patients with CoA. These findings demonstrate the clinical importance of exercise-induced hypertension and warrant additional study into the long-term consequences of exercise-induced hypertension and the potential beneficial role of early antihypertensive treatment in adult patients after CoA repair with exercise-induced hypertension.

The Impact of Anxiety Disorders on Assessment of Myocardial Ischemia and Exercise Stress Test Performance

To evaluate the sensitivity of electrocardiogram (ECG) versus single photon emission computed tomography (SPECT) assessments of ischemia in patients with anxiety disorders (AD) and the extent to which patients exhibit poorer exercise performance, compared with patients without AD. Patients referred for nuclear exercise stress testing (N = 2271) underwent a structured psychiatric interview (PRIME-MD) to assess for AD. Exercise performance parameters were assessed during ECG treadmill testing, after which patients underwent SPECT imaging. Analyses revealed that patients with AD exhibited lower peak exercise systolic blood pressure and rate pressure product than patients without AD. When major depressive disorder was included as an additional covariate, the previous results became trends. Results also indicated a lower rate of electrically positive ecg tests and a higher rate of false-negative diagnoses of myocardial ischemia according to ecg among patients with AD. Including major depressive disorder as a covariate rendered the effects of ad nonsignificant. There was no evidence of reduced exercise performance in patients with AD. Findings suggest that AD may be associated with mild impairments in cardiovascular exercise reactivity and may also alter the detection of myocardial ischemia using ecg assessments in patients referred for exercise stress testing. However, the influence of AD appears to be moderated by comorbid depression. Results suggest that exercise test performance and detection of ischemia may be influenced by mood and/or anxiety disorders and that greater efforts should be made to include routine mood and/or anxiety disorder screening as part of exercise stress testing protocols.

Relation of flow-mediated dilation to global arterial load: Impact of hypertension and additional cardiovascular risk factors

BackgroundEndothelial dysfunction may be related to increased left ventricular (LV) mass due to an association between endothelial dysfunction with increased arterial load. Therefore, we evaluated whether brachial artery flow-mediated dilation (FMD) is related to global arterial load. MethodsPulse pressure/stroke index (PP/SVi, global arterial stiffness, prognostically validated), stroke volume/PP (SV/PP, global arterial compliance), and % of the predicted SV/PP by heart rate, age and body weight (confounder-adjusted global compliance, prognostically validated) were used as LV geometry-related indices of global arterial load. ResultsCompared to normotensive participants (NT, n=50), those with hypertension (HTN, n=51) had lower FMD (8.3%±5.4 vs. 12.8%±6.5), higher PP/SVi (1.24±0.34 vs. 1.04±0.28mmHg m2/ml), higher LV mass and higher relative wall thickness (all p<0.01); in contrast, SV/PP and % of predicted SV/PP did not differ between NT and HTN (all p>0.1). Impaired FMD was 3–4-fold more prevalent than LV hypertrophy or increased arterial load both in NT and in HTN. Within NT and HTN separately, PP/SVi, SV/PP and % of predicted SV/PP were comparable among tertiles of FMD. Only in NT, lower FMD was associated with higher peak exercise systolic BP (p<0.05). In multivariable regression models, FMD was not associated with indices of arterial load independently (all p>0.1). ConclusionsIn young-to-middle-age subjects with cardiovascular risk factors, impaired FMD is more prevalent than traditional preclinical manifestation of cardiovascular disease, and may exist independent to increased arterial load. Thus, endothelial dysfunction assessment may refine cardiovascular risk profile and risk-reduction strategies based on detection of traditional target organ damage.

Relation of ventricular-vascular coupling to exercise capacity in ischemic cardiomyopathy: a cardiac multi-modality imaging study

The purpose of this study was to examine the relationship between noninvasive measurements of ventricular-vascular coupling (VVC) with exercise tolerance, and compared the value of VVC versus other traditional determinants of exercise capacity in this population. 43 patients with ischemic CMP (age 59 +/- 9 years, mean EF 24 +/- 8%) underwent cardiopulmonary exercise testing, echocardiography and cardiac magnetic resonance (CMR). VVC was defined non-invasively by the ratio of ventricular systolic elastance (Ees) to the arterial elastance (Ea), where Ees = end-systolic pressure/end-systolic volume index and Ea = end-systolic pressure/stroke volume index. VVC significantly correlated with baseline heart rate (HR), peak exercise systolic blood pressure, maximum oxygen consumption (MVO(2)) and peak O(2) pulse (MVO(2)/HR). A higher VVC was associated with higher LVEF and RVEF but showed inverse relation to mitral E wave velocity. Univariate predictors of MVO(2) are baseline HR, chronotropic reserve, VVC and aortic distensibility; whilst mitral E wave velocity, LVEF, VVC, Ees significantly correlated with peak O(2) pulse. By stepwise multivariate analysis, VVC remained the only independent predictor of peak O(2) pulse. Ventricular-vascular coupling at rest may be a clinically important parameter in predicting exercise capacity in patients with advanced heart failure, and may become an additional target for therapeutic interventions.

A randomized, double‐blind, placebo‐controlled study to determine the effects of valsartan on exercise time in patients with symptomatic heart failure with preserved ejection fraction

AimsTo determine whether valsartan improves treadmill exercise time, in patients with symptomatic heart failure with a preserved ejection fraction (HFPEF), compared with placebo.Methods and resultsIn this multicentred, double-blind, 14-week study, patients were randomized to receive valsartan (V) 80 mg or placebo (P) once daily on top of background medications. The dose of valsartan was force-titrated up to 320 mg. A total of 152 patients were randomized (V = 70, P = 82). Most patients had well-controlled hypertension (V = 91.2%, P = 89.0%) (mean baseline systolic BP ∼130 mmHg) and >50% were receiving an angiotensin-converting enzyme inhibitor and/or beta-blocker (V = 57.4%, P = 54.9%). The mean ejection fraction at baseline was 70.48% in the placebo group (n = 64) and 71.52% in the valsartan group (n = 79). Valsartan had no significant effect on exercise time (primary variable), gas exchange variables, 6 min walk test distance, exertion-related symptoms, brain natriuretic peptide levels, echocardiographic parameters, or quality-of-life scores. Valsartan significantly lowered peak exercise systolic BP (−13.1 mmHg vs. placebo; P < 0.001) and improved ratings of perceived exertion (Borg score) (−0.69 vs. placebo; P = 0.008).ConclusionIn this population, which predominantly included patients with well-controlled hypertension and symptomatic HFPEF, addition of valsartan did not increase exercise time within 14 weeks. However, valsartan 320 mg reduced blood pressure and improved symptoms of perceived exertion (Borg score) during exercise and was generally well-tolerated.

Adjuvant Trastuzumab Induces Ventricular Remodeling Despite Aerobic Exercise Training

To examine the effect of aerobic training in mitigating trastuzumab-mediated left ventricular (LV) remodeling in women with human epidermal growth factor receptor 2 (HER2)-positive breast cancer. Seventeen women (53 +/- 7 years) with HER2-positive breast cancer did aerobic training during the first 4 months of adjuvant trastuzumab. Peak oxygen consumption and magnetic resonance imaging assessment of LV volumes, mass, and rest and peak (dobutamine stress) ejection fraction were assessed before and after 4 months of trastuzumab. Participants attended 59% +/- 32% of prescribed exercise sessions at 78% +/- 6% of peak heart rate. Peak exercise heart rate, systolic and diastolic blood pressure, power output, and oxygen consumption were not different after training (all P-values > 0.05). Exercise adherence predicted change in peak oxygen consumption (r = 0.77; P = 0.000). Resting end-diastolic (pre: 120 +/- 23 mL versus post: 133 +/- 16 mL) and end-systolic volumes (pre: 44 +/- 12 mL versus post: 55 +/- 11 mL) and mass (pre: 108 +/- 21 g versus post: 114 +/- 18 g) increased, whereas ejection fraction (pre: 64% +/- 4% versus post: 59% +/- 4%) decreased from baseline to post-intervention (all P-values < 0.05). Peak ejection fraction was lower after 4 months (pre: 79 +/- 4 versus post: 76 +/- 6%; P = 0.087). Initiation of adjuvant trastuzumab therapy is associated with LV cavity dilation and reduced ejection fraction despite aerobic exercise training. The long-term consequences of trastuzumab-induced LV remodeling and the means to prevent LV dysfunction require further study.

Exercise Testing is Useful to Screen for Residual Coarctation in Children

Twenty-seven children (ages 8 to 18 years) who had a history of successful coarctation repair (mean transisthmic Doppler gradient [TI-D] <20 mmHg at rest) and had not received antihypertensive medications underwent echocardiogram at rest and immediately following peak exercise with a standard treadmill test. All were normotensive or had isolated systolic hypertension at rest. Right arm-ankle (RA-A) systolic blood pressure (SBP) difference and TI-D were measured. Eleven children (41%) demonstrated exercise-induced hypertension (peak exercise SBP >98th percentile per body surface area) and 17 (63%) had a mean TI-D > or =40 mmHg. Eight underwent MRI or angiography; a residual coarctation (RCoA) was confirmed in three and excluded in five. RCoA was excluded in three other children who were normotensive at rest and had normal postoperative echocardiographic findings. No individual test (SBP, RA-A SBP, TI-D) at rest or with exercise testing was statistically useful to identify RCoA. However, the requirement for a RA-A SBP difference > or =20 mmHg and a TI-D > or =40 mmHg during exercise testing was a useful screen: RCoA was present in three of five children who fit these criteria but was absent in six of six who did not.

Arm exercise testing predicts clinical outcome

Treadmill exercise testing provides prognostic and clinical information that is not available for patients with lower extremity disabilities who undergo pharmacologic stress tests. We sought to determine whether arm ergometer (AXT) exercise capacity in resting metabolic equivalents (METs) and hemodynamic and electrocardiographic responses to AXT are predictors of survival, myocardial infarction (MI), or coronary revascularization, individually or as a composite. A prospective cohort of 359 veterans aged 63 +/- 11 (SD) years, who were unable or unwilling to perform treadmill exercise, underwent AXT stress testing for clinical reasons between 1997 and 2002 and were followed for 63 +/- 24 months to an end point of death or December 31, 2006. Average annual mortality, MI, revascularization, and combined event rates were 5.2%, 1.7%, 2.2%, and 7.1%, respectively. By univariate analysis, AXT METs were highly predictive of survival (P < .01; hazard ratio 0.58, 95% confidence interval 0.46-0.70). A greater delta (peak-rest) heart rate, peak exercise systolic blood pressure, and rate pressure product were associated with survival and event-free outcome (all P < .02). A positive exercise electrocardiogram was predictive of death, revascularization, and combined events (all P < .01), and borderline predictive of MI (P = .058). By Wald chi(2) analysis, age, clinical variables, exercise capacity in METs, a positive exercise electrocardiogram, and delta heart rate all had statistically significant incremental prognostic value (P < .05) for survival. In older veterans with lower extremity disabilities and more comorbidities than most study populations, arm exercise capacity, delta heart rate, and a positive electrocardiogram were independently predictive of survival and/or adverse cardiovascular outcomes.

Exercise Blood Pressure Response, Albuminuria, and Arterial Stiffness in Hypertension

Background A hypertensive response to exercise is associated with high cardiovascular risk, whereas the data about its relation to surrogates of subclinical atherosclerosis are scarce. We investigated the relationships of a hypertensive response to exercise with urinary albumin excretion and arterial stiffness in hypertensives. Methods There were 171 untreated males (mean age 52 years, all Caucasian) with stage I-II essential hypertension and a negative treadmill exercise test divided into those with a hypertensive response to exercise (n = 48) (peak exercise systolic blood pressure ≥210 mm Hg) and to those with normal blood pressure response (n = 123). Albumin-to-creatinine ratio values were determined as the mean of 3 nonconsecutive morning spot urine samples, and arterial stiffness was evaluated on the basis of carotid-to-femoral pulse wave velocity. Results Patients with a hypertensive response to exercise compared with those with normal blood pressure response exhibited greater log albumin-to-creatinine ratio (1.52 ± 0.59 vs 0.97 ± 0.33 mg/g) and higher pulse wave velocity (8.7 ± 1.6 vs 7.7 ± 1.2 m/s), independent of potentially confounding demographic and clinical factors. Resting systolic blood pressure (odds ratio [OR] 1.11, 95% confidence interval [CI], 1.06-1.16), body mass index (OR 1.12, 95% CI, 1.02-1.23), resting heart rate (OR 0.96, 95% CI, 0.93-0.99), and albumin-to-creatinine ratio (OR 7.45, 95% CI, 2.54-21.83) were independently associated with a hypertensive response to exercise. Conclusion A hypertensive response to exercise is related to augmented albumin-to-creatinine ratio and arterial stiffness, reflecting accelerated subclinical atherosclerosis. The association of albumin excretion with exercise blood pressure response suggests that albuminuria constitutes an important factor in the interpretation of the hypertensive response to exercise-associated risk.

Increased cardiovascular risk in patients with a hypertensive response to exercise may be explained by masked hypertension

Background A hypertensive response to exercise (HRE; defined as normal clinic blood pressure [BP] and exercise BP g210/105mmHg in men or g190/105mmHg in women) independently predicts incident hypertension and cardiovascular mortality. The mechanisms remain unclear but may be related to masked hypertension. This study aimed to assess the prevalence of masked hypertension and cardiovascular risk factors, including aortic reservoir function, in patients with a HRE. Methods Comprehensive clinical and echocardiographic evaluation (including central BP, aortic reservoir pressure, aortic pulse wave velocity by tonometry) and 24 hour ambulatory BP monitoring (ABPM) were performed in 81 untreated patients with HRE (aged 54p9 years; 60% male; free from coronary artery disease). Masked hypertension was defined as ABPM systolic BP (SBP) g130 mmHg and clinic BP l140/90 mmHg. Results Masked hypertension was present in 50 patients (62%). These patients had higher left ventricular (LV) mass index (92.1p17.8 g/m2 versus 77.2p17.9g/m2; p=0.01) aortic reservoir pressure (104p9mmHg versus 97p10mmHg; p=0.001) and exercise SBP (226p15mmHg versus 210+15mmHg; pl0.001), despite no significant difference in aortic pulse wave velocity or central pulse pressure (pg0.05 for both). Aortic reservoir pressure was significantly correlated with peak exercise SBP (r=0.34; p=0.002). The strongest independent determinant of LV mass index was the pressure of masked hypertension (b=0.37; p=0.001) , ConclusionsAortic reservoir pressure is significantly elevated, and masked hypertension highly prevalent in HRE patients with a normal resting office BP. This may help to explain increased risk in patients with a HRE and clinicians should suspect masked hypertension in this population.

Effect of losartan on exercise tolerance and echocardiographic parameters in patients with mitral regurgitation

The aim of this study was to assess the effects of losartan treatment on exercise tolerance and echocardiographic parameters in patients with mitral regurgitation (MR) secondary to mitral valve prolapse or rheumatic heart disease. Twenty-seven patients (14 males, 13 females, mean age 51+/-11, range 21-76) with moderate MR due to mitral valve prolapse or rheumatic heart disease were examined by means of Doppler echocardiography. The subjects were submitted to treadmill exercise tests using the modified Bruce protocol at baseline, after six hours and after the six-week treatment period to be evaluated based on their exercise tolerance. Mitral Regurgitant Volume (MRV), effective regurgitant orifice diameter, left atrial volume, left ventricle (LV) end-diastolic volume index, LV end-systolic volume index, LV ejection fraction (LVEF), left ventricle mass index were calculated at baseline and after six weeks of treatment with single dose of losartan (50 mg/day). Total treadmill exercise time increased from 477.7+/-147.9 to 535.7+/-149.0 seconds after six hours (p<0.01) and to 559.6+/-142.8 seconds after six weeks of treatment. Also, metabolic equivalent values increased following six hours of first dose and six weeks of losartan treatment (from 10.9+/-2.9 to 11.8+/-3.1, p=0.006 and 12.4+/-3.1, p=0.002; respectively). However, peak exercise systolic blood pressure (BP) was reduced after six hours and six weeks of treatment, and resting diastolic BP did not change after six hours but reduced at the end of the treatment period. MR volume decreased significantly from 29.3+/-14.1 ml to 25.1+/-14.8 ml, (p=0.025) without significant change in regurgitant orifice diameter (0.72+/-0.37 cm vs. 0.66+/-0.37 cm, p=NS), left atrium diameter and area while LVEF increased from 51.70+/-13.37 to 54.11-11.75 (p=0.015) with losartan. We conclude that the angiotensin II receptor antagonist losartan improves exercise tolerance and echocardiographic parameters in patients with moderate MR.

Abstract 3109: Exaggerated Blood Pressure Response During Treadmill Test is Accompanied by a State of Pronounced Albuminuria, Hypoadiponectinemia and Increased Asymmetric Dimethylarginine Levels in Essential Hypertension

Introduction: A hypertensive response to exercise (HRE) is associated with high cardiovascular risk, whereas the data regarding its relation to markers of atherosclerosis progression are currently scarce. Hypothesis: Urinary albumin excretion, expressed as the albumin to creatinine ratio (ACR), asymmetric dimethylarginine (ADMA) levels, and adiponectin may be correlated with HRE in essential hypertensives. Methods: Our population of 109 newly diagnosed untreated non-diabetics with stage I to II essential hypertension [76 men, mean age =52 years, office blood pressure (BP) = 146/94 mmHg] with a negative treadmill exercise test (Bruce protocol) were divided into those with HRE (n=34) (peak exercise systolic BP ≥ 210mmHg in men and ≥190 mmHg in women) and to those without HRE (n=75). In all subjects ACR values were determined as the mean of two non-consecutive morning spot urine samples and venous blood samples were drawn for estimation of adiponectin and ADMA concentrations. Results: Patients with HRE compared to those without HRE were older (55 ± 9 vs 51 ± 9 years, p&lt;0.05), had greater 24-h systolic BP (141 ± 13 vs 132 ± 12 mmHg, p&lt;0.05), while did not differ regarding metabolic profile and left ventricular mass index (p = NS). Patients with HRE compared to those without HRE exhibited greater levels of ADMA (0.62 ± 0.05 vs 0.54 ± 0.04 μ mol/l, p&lt;0.0001) and ACR (61.4 ± 12 vs 15.2 ± 2.2 mg/g, p&lt;0.0001), whereas had lower adiponectin values (6.1 ± 1.4 vs 9.3 ± 2.1 μg/ml, p&lt;0.0001), independently of confounders. In the total population, peak exercise systolic BP was related to 24-h systolic BP (r=0.239, p&lt;0.05), ACR (r=0.432, p&lt;0.0001), ADMA (r=0.260, p=0.007), and negatively associated with adiponectin (r = −0.216, p&lt;0.05). Multiple regression analysis revealed that 24-h systolic BP (b=0.232, p=0.023), male sex (b=0.240, p=0.029) and ACR (b=0.450, p&lt;0.0001) were independent predictors of peak exercise systolic BP. Conclusions: In essential hypertension, a HRE is associated with hypoadiponectinemia, augmented ADMA and ACR values, reflecting activation of diverse pro-atherosclerotic pathways. These findings suggest that treadmill exercise testing could be an additional tool to identify hypertensive patients with pronounced cardiorenal vascular dysfunction.

Stress testing response in women heterozygous for familial hypercholesterolemia

We evaluated 62 exercise treadmill tests (ETTs) in equal numbers of heterozygous for familial hypercholesterolemia (hFH) and healthy (HLY) women, matched for age, baseline systolic and diastolic blood pressure (BP) and baseline heart rate (HR), using the Bruce protocol. Both groups had similar rate pressure product (RPP) and workload in metabolic equivalents (METs) (27,563 ± 3124 vs. 29,090 ± 4077, p = 0.103 and 11.2 ± 1.7 vs. 11.5 ± 1.8, p = 0.473, respectively). Women with hFH had lower delta (difference of peak to baseline) and peak exercise systolic and diastolic BP (systolic: 48 ± 12 vs. 58 ± 17 mmHg, p = 0.010 and 167 ± 19 vs. 177 ± 17 mmHg, p = 0.042, respectively; diastolic: 11 ± 7 vs. 15 ± 7 mmHg, p = 0.028 and 85 ± 7 vs. 91 ± 7 mmHg, p < 0.001, respectively). Furthermore, women with hFH had higher delta percentage (%) of HR, compared to HLY; (106 ± 25 vs. 95 ± 20, p = 0.047). In conclusion, hFH women possibly have an inadequate rise in systolic BP during ETT. Diastolic BP increased more in the HLY than in the hFH group, but still remained within normal limits. These findings may reflect preclinical changes of atherosclerosis in hFH women, however further research should be undertaken.

REPLY FROM DRS. BRASSARD AND POIRIER

To the Editor : We would like to thank Dr. Broderick ([2a][1]) for his interest and thoughtful comments regarding our manuscript. We agree that sympathetic dominance should not be ruled out for the increased (or preserved) exercise capacity observed in our subjects with high peak systolic blood

Elevated peak exercise systolic blood pressure is not associated with reduced exercise capacity in subjects with Type 2 diabetes

Subjects with Type 2 diabetes without cardiovascular disease have a reduced exercise capacity compared with nondiabetic subjects. However, the mechanisms responsible for this phenomenon are unknown. The purpose of this study was to evaluate the impact of exercise systolic blood pressure (SBP) response on diverse exercise tolerance parameters in Type 2 diabetic subjects. Twenty-eight sedentary men with Type 2 diabetes were recruited for this study. Subjects were treated with oral hypoglycemic agents and/or diet. Evaluation of glycemic control and peak exercise capacity were performed for each subject. The subjects were divided into two groups according to the median value of peak SBP (210 mmHg) measured in each subject. We observed a 13, 13, and 16% reduction in the relative peak oxygen uptake (V(O2 peak)), absolute V(O2 peak), and peak work rate in the low- compared with the high-peak SBP group [26.95 (SD 5.35) vs. 30.96 (SD 3.61) ml.kg(-1).min(-1), 2.5 (SD 0.4) vs. 2.8 (SD 0.6) l/min, and 169 (SD 34) vs. 202 (SD 32) W; all P < 0.05]. After adjusting for age, relative V(O2 peak) was still significantly different (P < 0.05). There were similar peak respiratory exchange ratio (RER) [1.20 (SD 0.08) vs. 1.16 (SD 0.07); P = 0.24] and peak heart rate [160 (SD 20) vs. 169 (SD 15) beats/min; P = 0.18] between the low- compared with the high-SBP group. No difference in glycemic control was observed between the two groups. The results reported in this study suggest that in subjects with Type 2 diabetes without cardiovascular disease, an elevated exercise SBP is not associated with reduced exercise capacity and its modulation is probably not related to glycemic control.

High Diastolic Blood Pressure During Exercise Is Associated With Hypercholesterolemia in Patients With Coronary Artery Disease

Evaluating blood pressure response during exercise rather than during rest might better detect a subtle impairment in relaxation of the resistance vessel in hypercholesterolemia. We examined the relation between serum cholesterol and blood pressure response during exercise in patients with coronary artery disease. One hundred and forty-eight consecutive patients with coronary artery disease were monitored during symptom-limited incremental exercise testing with a cycle ergometer. Cuff blood pressure was measured every minute during exercise testing with an automatic indirect manometer. Although there were no significant differences in systolic or diastolic blood pressure at rest between the patients with hypercholesterolemia (total cholesterol > or = 220 mg/dL, n = 39) and those without it (n = 109), the former reached a higher diastolic blood pressure at peak exercise (94.8+/-16.0 versus 87.8+/-12.9 mmHg, P = 0.007). The increase in diastolic blood pressure at peak exercise versus the resting value in the patients with hypercholesterolemia was 20.6+/-11.3 mmHg, and this was significantly higher than the increase in patients without hypercholesterolemia (14.8+/-11.8 mmHg, P = 0.009). However, there were no differences in the peak exercise systolic blood pressure and the magnitude of the increase in systolic blood pressure between the two groups. Among the patients with coronary artery disease in our study, we found that those with hypercholesterolemia had significantly higher diastolic blood pressure during exercise than those without hypercholesterolemia, strongly suggesting that patients with hyperlipidemia are at a higher risk of developing hypertensive complications.

Relationship between exercise systolic blood pressure and left ventricular geometry in overweight, mildly hypertensive patients.

To examine the association between the graded exercise systolic blood pressure (SBP) response and left ventricular (LV) geometric structure in patients with untreated mild hypertension. The study included 80 sedentary, overweight patients (43 female and 37 male) with unmedicated high normal blood pressure or stage 1-2 hypertension. An echocardiogram was used to determine LV mass and the relative wall thickness (RWT) in relation to the chamber dimension. Participants performed a maximal graded exercise test, and the SBP was recorded at workloads of 2, 4 and 6 metabolic equivalents and at peak exercise. Separate statistical models were used to determine the influence of LV mass indexed for height(2.7) (LVMIh) and RWT on submaximal exercise SBP and peak exercise SBP, controlling for resting SBP, age, gender, ethnicity and body mass index. A greater RWT was associated with a higher submaximal SBP level (P = 0.038). Neither LVMIh (P = 0.989) nor the interaction of RWT and LVMIh (P = 0.787) were related to the submaximal SBP. None of the main or interaction effects of RWT and LVMIh were associated with the peak exercise SBP level. Increases in RWT were associated with higher submaximal exercise SBP responses in a sample of overweight, unmedicated hypertensives. These results suggest that RWT is an important determinant of the association between cardiac mass and exercise SBP response.

The significance of hypertensive response to exercise as a predictor of hypertension and cardiovascular disease.

Several studies have shown that exaggerated blood pressure (BP) response to exercise can predict the development of hypertension and target organ damage, but others did not. The aim of this study was to evaluate the relationship between exaggerated BP response to exercise (ExBPR) and the development of hypertension or cardiovascular disease. We reviewed the charts of male subjects who, during the years 1991-1994, had a routine check up that included an exercise stress-test. For each subject, the following parameters were noted: age; body mass index (BMI); history of diabetes; cigarette smoking; family history of ischaemic heart disease and lipid profile. BP and heart rate at rest and during exercise were recorded as well. ExBPR was defined whenever peak exercise systolic BP or diastolic BP was over 200 mm Hg or 100 mm Hg respectively. We identified 73 males who exhibited ExBPR and matched them with a control group of 117 subjects with similar age who had a normal BP response. The mean age of the studied group was 42.6 years and the average follow-up was 5.7 years. Baseline characteristics were similar in both groups. During the follow-up we observed hypertension among 22% in those with ExBPR in contrast to 2.6% in the control group (P < 0.0001). In addition, more subjects of the ExBPR group required cardiovascular medications than of those in the control group (19.2% vs 4.3%, P = 0.0008). Thus, it seems that ExBPR predicts the development of hypertension and cardiovascular diseases. We therefore suggest that subjects with ExBPR should be followed more closely and be instructed for lifestyle modifications which may delay the development of such diseases.

Comparison of two calcium blockers on hemodynamics, left ventricular mass, and coronary vasodilatory in advanced hypertension

Dihydropyridine and nondihydropyridine calcium channel blockers (CCB) differ in pharmacologic characteristics. Few clinical studies distinguish effects of CCB as monotherapy. We conducted a comprehensive comparison of two CCB on patients with moderate to severe hypertension. Thirty patients with pretreatment diastolic blood pressures ≥100 mm Hg were randomly assigned to either nifedipine–GITS or verapamil-SR. Dose titration achieved a diastolic blood pressure of ≤95 mm Hg or a decrease of ≥15 mm Hg over 4 weeks. Clinic blood pressure (BP), 24-h ambulatory BP, exercise BP, left ventricular mass, systolic and diastolic function by echocardiography, and coronary flow reserve by split-dose thallium-201 imaging with adenosine were assessed at baseline, end of titration, 3 months and 6 months of treatment. Plasma renin activity, atrial natriuretic peptide, norepinephrine, and epinephrine were assayed. Both drugs caused similar reductions in clinic and 24-h ambulatory BP and similar reductions in left ventricular mass index. Compared to nifedipine–GITS, verapamil-SR produced a significantly lower resting and peak exercise heart rate. Nifedipine–GITS elicited a lower peak exercise systolic BP. At end titration nifedipine–GITS produced lower plasma atrial natriuretic peptide levels, no longer apparent by 6 months. Plasma norepinephrine was lower with verapamil-SR, also at end titration and at 3 months, but not at 6 months. Plasma epinephrine and plasma renin activity were unchanged by either drug. There was no difference for systolic or diastolic left ventricular function or coronary flow reserve between the two treatments. Once daily nifedipine–GITS and verapamil-SR are equally effective for reduction of arterial pressure in moderate to severe hypertension. Differences in their hemodynamic profiles and neurohormonal responses are consistent with preclinical pharmacologic characteristics. The clinical implications of their similarities and differences remain to be fully evaluated in outcome studies.