Normal Blood Pressure Response Research Articles

Exercise-induced abnormal blood pressure responses are related to subendocardial ischemia in hypertrophic cardiomyopathy.

We examined by thallium-201 scintigraphy whether exercise-induced abnormal blood pressure response (BPR) is related to myocardial ischemia. Hemodynamic instabilities during exercise in patients with hypertrophic cardiomyopathy (HCM) are considered to be caused by abnormal reflex control of vascular resistance. In 105 patients with HCM, exercise thallium scintigraphy was performed by means of a multistage, symptom-limited bicycle ergometer exercise test. Eighty-eight patients had normal BPR (> or = 25 mm Hg from baseline to peak exercise), and 17 had abnormal BPR (<25 mm Hg). Clinical characteristics including age, the prevalence of obstruction, New York Heart Association functional class and echocardiographic measurements were similar between the two groups. Left ventricular end-diastolic pressure was significantly higher in patients with abnormal BPR than in those with normal BPR (18+/-8 vs. 14+/-5 mm Hg, p < 0.05). Exercise-induced perfusion abnormalities including fixed and reversible perfusion defects, and left ventricular cavity dilatation (LVCD) were identified in 72 (69%) of 105 study patients. Left ventricular cavity dilatation indicates subendocardial hypoperfusion and is a marker of diffuse subendocardial ischemia. The prevalence of fixed or reversible perfusion defects was similar between the two groups. Patients with abnormal BPR had the higher prevalence of LVCD as compared to those with normal BPR (47.1 vs. 10%, p < 0.0002). Multiple logistic regression analysis revealed that LVCD was independently associated with abnormal BPR (odds ratio 3.76, 95% confidence interval 1.61 to 8.76). Exercise-induced abnormal BPRs in patients with HCM are related to subendocardial ischemia during exercise.

Exaggerated blood pressure response at exercise in normotensive subjects: Demographic and stress performance characteristics

Background Exercise testing is an important diagnostic and prognostic procedure in the assessment of patients with hypertension. An exaggerated blood pressure response to exercise among normotensive subjects was found to be one of the best predictors of future hypertension. The demographic characteristics of patients with an exaggerated blood pressure response during exercise have not been adequately described. Methods and Results The demographic and stress performance characteristics of 2 groups of normotensive patients referred for exercise testing, one composed of patients with an exaggerated blood pressure response (group I, n = 146) and a group of patients with a normal blood pressure response (group II, n = 439) were prospectively compared. Patients in group I were older than those in group II (54 ± 12 vs 51 ± 13 years, P < .05). More men than women were found in both groups, yet significantly more in group I than in group II (83% vs 69% P < .001). Significantly more among the patients in group I had a higher level of education and were of Western origin than those in group II ( P < .01). The resting systolic and diastolic blood pressures were higher in group I than in group II (131 ± 18 vs 119 ± 14 mm Hg, P < .001, and 81 ± 8 vs 76 ± 7 mm Hg, P < .001, respectively). The patients in group I achieved a higher percentage of the maximal predicted heart rate (88 ± 7 vs 85 ± 9 beats/min, P < .01). No significant differences were found between the groups in the duration of stress test and effort ischemia. Conclusions Patients with a hypertensive blood pressure response during stress testing have specific demographic and exercise characteristics. (Am Heart J 1998;136:499-503.)

Venous dysfunction and the change of blood viscosity during head-up tilt.

The precise stimulus that induces vasovagal syncope is still unclear. We have previously demonstrated that the peripheral distribution of blood volume (venous pooling) is a strong predictor of tilt induced vasovagal reaction. We hypothesized that an increase in venous pooling during tilt accentuates the measured increase in blood viscosity. This hypothesis is based on the previously demonstrated increase in venous pressure and subsequent increase in transcapillary fluid transudation during tilt. The increased blood viscosity, in turn, increases vascular shear rate, which may alter the vasoconstrictive and other cardiovascular responses to decreased preload. We measured blood viscosity (supine and tilt) in 56 patients with a history of orthostatic intolerance (37 with venous pooling [VP] and 19 without venous pooling [non-VP]). VP and non-VP were separated into subgroups based on blood pressure and heart rate response to tilt. There was a positive correlation between blood viscosity and plasma aldosterone in the supine. In the group as a whole, neither supine blood viscosity nor its increase during tilt differed between VP and non-VP. However, the tilt induced increase of blood viscosity was significant only in patients with tilt provoked tachycardia plus normal blood pressure response in VP group. We suggest that the increase of blood viscosity in this group led to the normal blood pressure response. The positive correlation between supine blood viscosity and supine plasma aldosterone indicates that the normal blood pressure response in this group possibly was via stimulation of the renin-angiotensin-aldosterone system.

Prospective prognostic assessment of blood pressure response during exercise in patients with hypertrophic cardiomyopathy.

Previous studies revealed that an abnormal blood pressure response (ABPR) during exercise was common in young hypertrophic cardiomyopathy (HCM) patients and was associated with a family history of premature sudden cardiac death (SCD). This study was performed prospectively to assess the prognostic significance of blood pressure response during exercise in young patients with HCM. Maximum symptom-limited treadmill exercise testing with continuous blood pressure monitoring was performed in 161 consecutive patients 8 to 40 years old (27+/-9). A normal blood pressure response, defined as an increase in the systolic pressure of at least 20 mm Hg from rest to peak exercise in the absence of a fall of >20 mm Hg from peak pressure, was seen in 101 (63%). In 60 (37%), the blood pressure response was abnormal. There was no significant difference in patients with normal blood pressure response and ABPR in terms of age, sex, follow-up, or recognized risk factors for SCD. During the follow-up period (mean, 44+/-20 months), SCD occurred in 12 patients: 3 (3%) in the normal blood pressure response group versus 9 (15%) in the ABPR group (P<.009). ABPR had a sensitivity of 75%, a specificity of 66%, a negative predictive value of 97%, and a positive predictive value of 15% for the prediction of SCD. There was no significant difference in the incidence of other recognized risk factors between patients with SCD and the survivors. A normal exercise blood pressure response identifies low-risk young patients with HCM. An ABPR identifies the high-risk cohort; the low positive predictive accuracy, however, indicates that further risk stratification is warranted.

Doppler Echocardiographic Indexes and 24-H Ambulatory Blood Pressure Data in Sedentary Middle-Aged Men Presenting Exaggerated Blood Pressure Response During Dynamical Exercise Test

Previous studies have pointed out that exaggerated blood pressure (BP) response during physical exercise could be an early marker of essential hypertension. Apparently some of the exaggerated BP responders present changes in the heart geometry and function that are usually found in the early course of the hypertensive disease. To evaluate the association between exaggerated BP response and these changes, we submitted 20 normotensive men presenting elevated BP response during bicycle exercise (hyperreactive group, systolic BP ≥ 220 mmHg at maximal workload) to 24-h ambulatory blood pressure monitoring (ABPM) and to two-dimensionally guided M-mode echocardiography and pulsed Doppler. The results from this group were contrasted with those of a comparable group, which otherwise, presented normal BP response during the same procedure (control group, systolic BP ≤ 210 mmHg at maximal workload). The ABPM measurements were normal and analogous between the two groups: the mean 24-h systolic blood pressure (SBP) was respectively 126·6 mmHg and 129·5 mmHg, diastolic blood pressure (DBP) 82·4 mmHg in both groups, and heart rate (HR), respectively 76·9 and 74·7 bpm. The univariate correlation (R) between the maximal BP response during bicycle exercise and BP measurements in the ABPM were in general weak, and as a whole, the hyperreactive group presented the weakest correlation coefficients. M-mode echocardiographic data such as the left ventricular mass index (LVMI, 80·10 vs. 81·11 g/m2), posterior wall and interventricular septal thickness (PWT, 8.8·0.6 vs. 8.6 <0.7 mm; IVST, 9.0·0.4 vs. 8.8·0.6) were also normal and comparable between the groups. LV systolic functional indexes such as fractional shortening (LVFS, 39·2.8 vs. 40·3.5 %) and ejection

Mechanism of exercise hypotension in patients with ischemic heart disease. Role of neurocardiogenically mediated vasodilation.

Exercise-induced hypotension in patients with coronary artery disease (CAD) has been considered to be due to an inability to achieve an adequate increase in cardiac output to match the demands of exercise. We investigated 10 consecutive patients (9 men and 1 woman; age, 38 to 71 years; mean, 52 years) with angiographically documented CAD and exercise-induced hypotension (EIH) (BPPeak < BPRest). Ten approximately age- and sex-matched patients with documented CAD and normal exercise blood pressure response (NBP) served as control subjects. Nine patients with EIH and all 10 control subjects underwent forearm plethysmography and radionuclide ventriculography (RNV) during semierect cycle exercise. Forearm vascular resistance (FVR) fell by 35 +/- 21% in exercise-induced hypotension patients versus an increase of 78 +/- 65% in patients with an NBP response (P < .0001). Left ventricular ejection fraction increased by 5.1 +/- 7.5% in the group with EIH versus a fall of 4.1 +/- 6.2% in the control group (P = .004). Cardiac output at peak exercise (RNV) increased by 2.2 +/- 0.89-fold in the group with EIH versus 1.49 +/- 0.47-fold in the control group (P = .04). The tenth patient in the group with EIH underwent invasive hemodynamic evaluation during erect exercise. Systolic blood pressure fell (136/80Rest to 50/40Peak) and cardiac output (Fick) tripled, whereas calculated systemic vascular resistance decreased by a factor of 10. Successful angioplasty to an isolated circumflex lesion resulted in resolution of symptoms and abnormal hemodynamic responses during exercise. Abnormal vasodilation associated with a normal or even increased rather than decreased cardiac output response appears to be an important mechanism underlying EIH in some patients with CAD. In the present study, this appears to have been the dominant mechanism in 8 and contributory in 2 of the consecutive patients studied.

Abnormal Valsalva blood pressure response in dilated cardiomyopathy: Association with “pseudonormalization” of echocardiographic Doppler transmitral filling velocity pattern

In patients with dilated cardiomyopathies, the presence of an abnormal blood pressure response to the Valsalva maneuver has been shown to correlate well with increased left-sided filling pressures. The presence of a “pseudonormalized” early peak to late peak velocity ( E A ) ratio on echocardiographic Doppler transmitral filling pattern has also been correlated with increased left ventricular end-diastolic pressures in these patients. Since both abnormal blood pressure response to the Valsalva maneuver and a “pseudonormalized” Doppler transmitral E A ratio probably represent elevated left ventricular filling pressure, we postulated that there would be a positive correlation between the two in a group of patients with dilated cardiomyopathy and abnormal systolic function. Twenty-five consecutive male patients with New York Heart Association (NYHA) class II to IV heart failure and dilated cardiomyopathy were included. Patients with abnormal blood pressure responses to Valsalva had significantly larger peak early (E) velocities, smaller peak late (A) velocities, and larger E A ratios compared with patients with normal responses. E A ratio <1.0 was present in eight (100%) of the eight patients with a normal blood pressure response to the Valsalva maneuver and E A ratio >1.0 was present in 12 (71%) of 17 patients with an abnormal response ( p < 0.01). This correlation supports the hypotheses of the physiologic mechanisms of these phenomena and also provides two noninvasive methods of evaluating left-sided filling pressures useful in the diagnosis and treatment of congestive heart failure caused by dilated cardiomyopathy.

Neural control of cardiovascular responses and of ventilation during dynamic exercise in man.

1. Nine subjects performed dynamic knee extension by voluntary muscle contractions and by evoked contractions with and without epidural anaesthesia. Four exercise bouts of 10 min each were performed: three of one-legged knee extension (10, 20 and 30 W) and one of two-legged knee extension at 2 x 20 W. Epidural anaesthesia was induced with 0.5% bupivacaine or 2% lidocaine. Presence of neural blockade was verified by cutaneous sensory anaesthesia below T8-T10 and complete paralysis of both legs. 2. Compared to voluntary exercise, control electrically induced exercise resulted in normal or enhanced cardiovascular, metabolic and ventilatory responses. However, during epidural anaesthesia the increase in blood pressure with exercise was abolished. Furthermore, the increases in heart rate, cardiac output and leg blood flow were reduced. In contrast, plasma catecholamines, leg glucose uptake and leg lactate release, arterial carbon dioxide tension and pulmonary ventilation were not affected. Arterial and venous plasma potassium concentrations became elevated but leg potassium release was not increased. 3. The results conform to the idea that a reflex originating in contracting muscle is essential for the normal blood pressure response to dynamic exercise, and that other neural, humoral and haemodynamic mechanisms cannot govern this response. However, control mechanisms other than central command and the exercise pressor reflex can influence heart rate, cardiac output, muscle blood flow and ventilation during dynamic exercise in man.

Increased response of diastolic blood pressure to exercise in patients with coronary artery disease: an index of latent ventricular dysfunction?

To determine whether an abnormal response of diastolic blood pressure during treadmill exercise stress testing correlated with the number of obstructed vessels and with left ventricular systolic function in patients with coronary artery disease. Diastolic blood pressure was measured invasively during exercise stress testing and coronary angiograms and left ventriculograms were obtained at rest in patients with coronary artery disease. The abnormal (> or = 15 mm Hg) diastolic blood pressure response was compared with the number of obstructed coronary arteries and with left ventricular systolic function. Two tertiary referral centres. 50 consecutive patients (mean age 57 years) with coronary artery disease. The increase in diastolic blood pressure during exercise and its correlation with the appearance and disappearance of ST segment deviation, resting left ventricular systolic function, and the number of obstructed coronary arteries. Group 1: 10 (20%) patients (three with one, four with two, and three with three vessel coronary artery disease) (mean (SD) age 54.7 (12) years) had an abnormal diastolic blood pressure response that appeared 1.2 (0.3) min before ST segment deviation and became normal 0.9 (0.3) min after the ST segment returned to normal. Group 2: 40 (80%) patients (12 with one, 16 with two, and 12 with three vessel coronary arteries disease) (aged 56.8 (8.2) years) had a normal diastolic blood pressure response to stress testing. The ejection fraction (46.3 (5)%) and cardiac index (2.6 (0.1) 1/min/m2) in group 1 were less than in group 2 (61.6 (4.2)% and 3.8 (0.3) 1/min/m2 respectively, p < or = 0.001). The end systolic volume was greater in group 1 than in group 2: 38.7 (0.7 ml/m2 v 28.2 (2.1) ml/m2, p < or = 0.001. In patients with coronary artery disease an abnormal increase in diastolic blood pressure during exercise stress testing correlated well with left ventricular systolic function at rest but not with the number of obstructed coronary arteries. The abnormal response of diastolic blood pressure probably reflects deterioration of myocardial function.

Is Absolute Hypovolemia a Risk Factor for Vasovagal Response to Head‐Up Tilt?

To test the hypothesis that hypovolemia is associated with an increased incidence of vasovagal syncope during head-up tilt (HUT) 45 patients with history of syncope or presyncope were studied. Blood volume (radio-iodinated serum albumin) was determined, then subjects underwent a graded HUT (from 15 degrees-60 degrees HUT) with cuff blood pressure and ECG monitoring. All patients were kept on their own medications during evaluation. Thirty patients (12 male, 18 female, mean age 50 +/- 19 [SD] years) had hypovolemia, defined as blood volume < 90% of lab normal for corresponding sex, while 15 patients (7 male, 8 female, mean age 52 +/- 21 years) were normovolemic with blood volume ranging from 91%-110% of sex-matched normal subjects. The normovolemic patients served as controls. During HUT, a vasovagal response was elicited in 5 of the 30 hypovolemics and in 4 of the 15 normovolemic (16.7% and 26.7%, respectively, P = NS). In those who developed vasovagal response, the changes of heart rate and blood pressure during HUT were not significantly different between hypovolemics and normovolemics, neither at the endpoint (vasovagal response) nor immediately before the development of the vasovagal response. In patients with nonvasovagal events, four types of hemodynamic responses to tilt were observed: normal blood pressure response associated with normal heart rate increase, normal blood pressure response in association with accentuated increase in heart rate, orthostatic hypotension with normal acceleration of heart rate, and orthostatic hypotension with accelerated increase in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Is there a relationship between exercise systolic blood pressure response and left ventricular mass? The Framingham Heart Study.

To assess the association between an exaggerated exercise systolic blood pressure response and the occurrence of left ventricular hypertrophy in healthy, normotensive individuals. Cross-sectional survey using M-mode echocardiography to measure left ventricular mass and to detect left ventricular hypertrophy. The Framingham Heart Study. Eight-hundred sixty men and 1118 women were studied who were free of cardiovascular or pulmonary disease, who were not taking any antihypertensive or cardiovascular medications, and who successfully achieved at least 90% of their age-predicted maximum heart rate during a monitored exercise treadmill test. All subjects had normal baseline and exercise electrocardiograms. Men with a peak exercise systolic blood pressure of 210 or more and women with a peak exercise systolic blood pressure of 190 or more were considered to have an "exaggerated" blood pressure response; 122 men and 67 women met these criteria. Subjects with an exaggerated exercise systolic blood pressure response had 10% higher left ventricular mass than those with a normal exercise systolic blood pressure response (in men: 115 +/- 25 compared with 105 +/- 24 g/m, P less than 0.001; in women: 86 +/- 22 compared with 73 +/- 16 g/m, P less than 0.001); they also had a higher prevalence of left ventricular hypertrophy (in men: odds ratio, 1.34, 95% CI, 1.00 to 1.80; in women: odds ratio, 2.12, CI, 1.48 to 3.03). After adjusting for age, resting systolic blood pressure, and body mass index, however, subjects with an exaggerated exercise systolic blood pressure response had only 5% higher left ventricular mass (in men: 111 +/- 2.1 compared with 106 +/- 0.8 g/m, P = 0.02; in women: 80 +/- 1.8 compared with 74 +/- 0.4 g/m, P = 0.002), and they no longer had a statistically increased prevalence of left ventricular hypertrophy (in men: odds ratio, 1.21, CI, 0.87 to 1.67; in women: odds ratio, 1.30, CI, 0.84 to 2.01). The apparent relation between exercise systolic blood pressure response and left ventricular mass is confounded by age, resting systolic blood pressure, and body mass; the degree of confounding is such that the biologic significance of this relationship should be questioned.

Abnormal vascular responses to supine exercise in hypertrophic cardiomyopathy.

Exercise hypotension has been documented in hypertrophic cardiomyopathy. It is not the result of an inability to augment cardiac output but instead relates to an inappropriate and exaggerated decrease in systemic vascular resistance at high work loads. To enable us to examine the behavior of the peripheral vasculature during exercise, 103 consecutive patients underwent maximal symptom-limited supine bicycle exercise with measurement of forearm blood flow. A minimum reduction of 12% from the basal value was defined as a normal response based on the study of 25 normal controls. In the patients, two patterns of forearm blood flow were observed. Sixty-four patients had an appropriate reduction in forearm blood flow of 40 +/- 16% from resting flow. In 39 patients, the forearm blood flow either failed to decrease or increased with exercise by 45 +/- 105% of the resting value. Patients with an abnormal forearm vasodilator response were younger (31 +/- 13 versus 46 +/- 14 years), and more of them had a family history of hypertrophic cardiomyopathy and sudden death than did those with a normal vasoconstrictor response (16 of 39 versus eight of 64). Left ventricular end-diastolic cavity dimensions were smaller in those with an abnormal forearm blood flow response, but other clinical, echocardiographic, and arrhythmic variables were similar. To assess the relation of abnormal peripheral vascular responses to erect exercise blood pressure response, patients underwent treadmill exercise testing with careful monitoring of systolic blood pressure response. Thirty-eight patients had significant exercise hypotension with failure of the systolic blood pressure to increase during progressive exercise (n = 6) or an abrupt decrease in systolic blood pressure (20-60 mm Hg) from the peak value (n = 32); 65 patients had a normal exercise blood pressure response, but 18 of these patients had an oscillation in systolic blood pressure of 10 mm Hg or more early in the recovery phase. Thirty-one of 39 patients with an abnormal forearm blood flow response demonstrated exercise hypotension during the erect exercise testing, and the remaining eight patients had a normal exercise blood pressure response; however, five of these eight had abnormal oscillations in blood pressure during recovery (r = 0.61, p less than 0.001). The relation of abnormal peripheral vascular responses to exercise hypotension confirms the observation of hemodynamic instability in patients with hypertrophic cardiomyopathy. The finding of abnormal vascular responses in patients known to be at increased risk (young age and a family history of hypertrophic cardiomyopathy and sudden death) suggests that hemodynamic mechanisms may be important in the occurrence of sudden death in hypertrophic cardiomyopathy.

Spectrum of orthostatic disorders: Classification based on an analysis of the short-term circulatory response upon standing

1. In 31 consecutively referred patients (20 females, 11 males) with overt or suspected orthostatic disorders, the changes in blood pressure and heart rate that occur in the first 2 min of standing were analysed. 2. Blood pressure was measured continuously by Finapres. The blood pressure and heart rate responses after 1-2 min of standing (early steady-state response) were used to classify the patients as follows: group I (n = 17, age 42 +/- 17 years), normal early steady-state blood pressure and heart rate responses; group II (n = 5, age 40 +/- 14 years), combination of normal early steady-state blood pressure and postural tachycardia; group III (n = 9, age 51 +/- 14 years), hypotensive orthostatic response with (4/9) or without (5/9) postural tachycardia. We examined whether additional information could be obtained by beat-to-beat analysis of the initial circulatory response (first 30 s). It was quantified by identifying the blood pressure trough and overshoot and the maximum heart rate and relative bradycardia. 3. The initial drop in systolic and diastolic blood pressures did not differ between the three groups. A recovery of blood pressure with a systolic and/or diastolic blood pressure overshoot was present in all group I and II patients, but was absent in all except two patients in group III. The initial maximum heart rate increase did not differ between the three groups. The relative bradycardia was less in groups II and III than in group I. 4. We conclude that analysis of the beat-to-beat blood pressure changes in the first 30 s after the onset of standing provides almost all the information that is necessary to determine abnormalities in orthostatic circulatory control.

Abnormal blood pressure response during exercise in hypertrophic cardiomyopathy.

To investigate the incidence of abnormal exercise blood pressure responses in hypertrophic cardiomyopathy (HCM) and the potential role of hemodynamic instability as a mechanism of sudden death, 129 consecutive patients with HCM underwent maximal symptom-limited treadmill exercise testing with blood pressure recording. Four patterns of blood pressure response were observed. Forty-three patients had significant exercise hypotension, with either a continuous fall in systolic blood pressure (n = 5) from the start of exercise or a sudden fall in systolic blood pressure (20-100 mm Hg; mean, 40 mm Hg) from the peak value (n = 38), 23 patients had a normal response during exercise but an abnormal blood pressure response in the recovery period, and the remaining 62 patients demonstrated a normal blood pressure response. Patients with exercise hypotension were younger (33 +/- 14 versus 46 +/- 14 years) and more of them had a family history of HCM and sudden death compared with those with a normal blood pressure response (15 of 43 versus 6 of 62 patients). Similarly, the 23 patients with abnormal recovery blood pressure responses were younger (43 +/- 16 versus 46 +/- 14 years) and had a higher incidence of a family history of sudden death (10 of 24 versus 6 of 62 patients). Left ventricular cavity dimensions were smaller in those with exercise hypotension, but 11 other clinical, echocardiographic, and arrhythmic variables were similar. To assess the mechanism of exercise hypotension, 14 patients who demonstrated exercise hypotension and 14 symptomatic patients with a normal exercise blood pressure response underwent invasive hemodynamic exercise testing.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise stress testing in blood pressure evaluation.

The purpose of this study was: (1) to confirm exercise stress testing as a standard in the diagnosis of hypertension, (2) to clarify which measurements during exercise testing are most reliable, and (3) to refine the definition of normal blood pressure response during ergometric exercise testing. Blood pressure response during maximal ergometric exercise testing was observed in 183 persons with no history of hypertension, 176 persons with borderline blood pressure readings, and 60 established hypertensives. Men and women had significantly different blood pressure response to exercise (P less than 0.05). Comparison of blood pressures at 100-watts workload, at peak exercise, and 5-minutes postexercise provided significant information for distinguishing between normal, borderline, and established hypertensive persons (P less than 0.025-0.001). Comparing the slopes of pulse rate versus blood pressure linear regression curves was not helpful. Regression equations generated for predicting correct blood pressure classification improved classification accuracy (compared with random classification) by 44.9 percent in men and by 66.8 percent in women. The results showed that ergometric stress testing in blood pressure evaluation is a safe and reliable procedure for aiding in a more accurate diagnosis of hypertension.

The significance of abnormal systolic blood pressure response during supine ergometer exercise and postexercise in ischemic heart disease, studied by exercise radionuclide ventriculography.

The prognostic value of abnormal postexercise systolic blood pressure (BP) response has not been investigated. Therefore, the significance of abnormal BP response during exercise and postexercise was examined in 169 patients with ischemic heart disease subjected to supine ergometer exercise gated equilibrium radionuclide ventriculography, coronary arteriography, and follow up averaging 3.6 years. Abnormal BP response during exercise (exertional "hypotension") was defined as 1) a failure of BP to rise by at least 11 mmHg or 2) an initial rise in BP but subsequent fall by more than 10 mmHg during exercise. Abnormal BP response during postexercise (postexercise "hypertension") was defined as an increase of more than 10 mmHg above the peak exercise BP. Of 169 patients, 51 (30%) had an abnormal BP response. Four types of BP response were identified: exertional "hypotension" (group 1a, n = 11), postexercise "hypertension" (group 1b, n = 30), exertional "hypotension" with postexercise "hypertension" (group 1c, n = 10) and normal BP response (group 2, n = 118). Both average exercise duration and peak heart rate were significantly lower in groups 1a, 1b and 1c than in group 2. The severity of exercise ST-segment depression was greater in groups 1b and 1c than in group 2. However, there was no significant difference in the severity of exercise ST-segment depression between group 1a and group 2. A decline in ejection fraction occurred more frequently in groups 1b and 1c than in group 2. Patients in groups 1a, 1b and 1c had more extensive coronary artery disease (CAD) than did patients in group 2. Medically treated patients with an abnormal BP response (groups 1a, 1b and 1c) had a poorer prognosis than did those with a normal BP response (group 2). These findings suggest that an abnormal BP response during supine exercise is infrequent, but is usually associated with impaired exercise tolerance and severe CAD. An abnormal postexercise BP response is also infrequent, but is more closely associated with evidence of myocardial ischemia and global left ventricular dysfunction than exertional "hypotension". In conclusion, postexercise "hypertension" has the same value as exertional "hypotension" as a predictor of poor prognosis.

Left ventricular exercise echocardiographic abnormalities in apparently healthy men with exertional hypotension

Of a total of 1,435 healthy untrained asymptomatic individuals referred for a routine periodic check-up, 23 subjects with exertional hypotension on upright bicycle stress testing were identified. All were male. This study assesses by means of echocardiography the responses to exercise of left ventricular (LV) volumes, ejection fraction and segmental LV contractility in these subjects. Exertional hypotension was defined as a decrease in systolic blood pressure to below the resting value at the end of stress test. Supine systolic blood pressure after exercise was significantly greater in the control group than in the study group (179 vs 121 mm Hg, respectively; p < 0.001); there was no significant intra- or intergroup difference in the resting values. In the study group end-systolic volume was 37 ml at rest and 35 ml after exercise; ejection fraction varied from 65% at rest to 63% after exercise. The sex- and age-matched control group with a normal systolic blood pressure response to exercise showed a shift from 35 to 23 ml and 65 to 77%, respectively (p < 0.01 and 0.001). Ejection fraction correlated well with radionuclide angiography values. Exertional hypotension was noted after both upright and supine exercise. The pattern of regional wall motion remained unchanged or was hypokinetic in 87% of the subjects; only 13% presented the normally expected hyperkinesia after exercise. This study demonstrates that exertional hypotension is accompanied by an abnormal LV performance.

Anti-sympathetic ganglia antibodies and postural blood pressure in IDDM subjects of varying duration and patients at high risk of developing IDDM.

We examined the sera of 94 subjects with insulin-dependent diabetes mellitus (IDDM) for the presence of complement-fixing sympathetic ganglia (CF-SG) antibodies. In a cross-sectional analysis (duration 0-43 yr), 22% had detectable CF-SG antibodies. Subjects at high risk for IDDM were also studied. Four groups were studied: group 1 (aged 4-64 yr) islet cell antibody-positive (ICA+) prediabetic subjects, 10 of 19 (53%) were CF-SG+; group 2 (aged 6-14 yr) ICA- prediabetic subjects (first-degree relatives of IDDM subjects with either transient hyperglycemia, impaired oral glucose tolerance, and/or first-phase insulin release after intravenous glucose tolerance testing), 4 of 9 (44%) were CF-SG+ (2 of the 4 ICA- CF-SG+ subjects have progressed to IDDM); group 3 (aged 1.5-43 yr) ICA+ IDDM subjects (less than or equal to 1 yr duration) 6 of 10 (60%) were CF-SG+; and group 4 (aged 8-59 yr) ICA- IDDM subjects (less than or equal to 1 yr duration), 2 of 11 (18%) were CF-SG+. All groups had increased CF-SG compared with controls. Postural blood pressure and simultaneous CF-SG antibody measurements were performed in 28 IDDM subjects. The drop in systolic blood pressure was greater in the CF-SG+ subjects (P less than .05), and the frequency of CF-SG was greater in the mean to -2SD group (P less than .03) when data were analyzed within mean +/- 2SD of the normal blood pressure response.

Evaluation of age, gender, heart rate and blood pressure changes and exercise conditioning on Doppler measured aortic blood flow acceleration and velocity during upright treadmill testing

To evaluate the effect of upright exercise on aortic peak flow acceleration and velocity, 60 normal subjects between 15 and 74 years of age were evaluated by continuous wave Doppler during treadmill stress testing using the Brace protocol. Subjects were divided into 3 age groups, each with 20 subjects: group 1, 21 ± 4 years of age (mean ± standard deviation), group 2, 36 ± 5 years and group 3, 58 ± 7 years. Periodic measurements of heart rate, blood pressure and Doppler blood flow velocity and acceleration were made before, during and after exercise. Continuous wave Doppler measurements were recorded from the suprasternal notch. The relation between Doppler aortic measurements and age, gender, normal heart rate and blood pressure responses during exercise, and exercise preconditioning, was evaluated. Age alone was significantly related (inversely) to immediate postexercise Doppler aortic peak blood flow peak acceleration (group 1, 55 ± 15, group 2, 46 ± 11 and group 3, 36 ± 9 m/s 2, p < 0.05) and peak velocity (1.1 ± 0.2, 1.0 ± 0.2 and 0.8 ± 0.2 m/s, respectively, p < 0.01). Gender, heart rate and blood pressure changes during exercise, as well as preconditioning, had no significant effect on these flow characteristics. Consequently, the effects of normal aging must be considered when using Doppler measurements of peak aortic acceleration and velocity in the evaluation of left ventricular function, e.g., to detect or exclude the presence of coronary artery disease.

Significance of abnormal blood pressure response during exercise-induced myocardial dysfunction after recent acute myocardial infarction

The relation between exercise left ventricular ejection fraction and blood pressure (BP) responses after an acute myocardial infarction (AMI) was investigated. Twenty-eight to 37 days after an uncomplicated AMI, 224 consecutive patients underwent exercise radionuclide angiography in the 40 ° semisupine position. In 180 patients (group A, 80%), BP increased more than 5 mm Hg every stage; in 44 patients, BP responses were abnormal; in 33 (group B, 15%), BP did not increase during 2 stages; in 11 (group C, 5%), it decreased more than 5 mm Hg after an initial increase. Ejection fraction did not differ significantly among the 3 groups at rest (51 ± 13 in group A, 50 ± 18 in group B, 47 ± 13 in group C [difference not significant]) or at peak exercise (51 ± 16% in group A, 46 ± 19% in group B, and 43 ± 16% in group C, [difference not significant]). Exercise-induced left ventricular failure or hemodynamic decompensation occurred in 22 patients. In these patients, ejection fraction at rest was 44 ± 19% and decreased to 35 ± 16% (p < 0.05) with exercise. Only 9 of these patients (41 %) had abnormal BP responses, with the other 13 (59%) showing a normal BP response. The 35 patients with abnormal BP responses in the absence of hemodynamic decompensation were asymptomatic, terminating exercise because of fatigue. The ejection fraction at rest and during exercise in these patients was similar to that in patients with normal BP responses. Thus, after a recent AMI, abnormal BP responses during exercise associated with clinical evidence of hemodynamic decompensation are related to myocardial dysfunction. However, in the absence of symptoms, such abnormal BP responses are not related to severity of left ventricular dysfunction, and in some patients may be ascribed to exertional reduction in systemic resistance.