In order to identify the hemodynamics of borderline essential hypertension, radionuclide angiography was performed before and after bolus injection of furosemide (40 mg i.v.) both at 3 min (i.e. before diuretic effect) and at 30 min (i.e. after diuretic effect) in 16 borderline (B) patients and in 14 age-matched WHO classification I-II essential hypertensives (H) patients. 14 age-matched normotensive (N) subjects were used as controls. B patients were further subdivided into two subgroups according to a cardiac index under or above 3 liter/min/m2 in basal conditions. Baseline hemodynamic characteristics showed higher values of mean arterial pressure (MAP) and systemic vascular resistance index (SVRI) in both H and B patients when compared with N subjects (p < 0.001). Furthermore, B and H patients exhibited lower values of left ventricular peak filling rate (PFR) than seen in N subjects (p < 0.01 and p < 0.05, respectively). H patients demonstrated higher peak systolic blood pressure/end-systolic volume ratio (PSP/ESV) than seen in N subjects (p < 0.05). PFR positively correlated with peak emptying rate (PER) only in N and B patients (p < 0.05). After furosemide administration, even though differences were observed in the absolute values, B and H patients showed similar hemodynamic patterns. Only the B subgroup with cardiac index (CI) > 3 liter (‘volume-dependent’ patients) showed a decrease in left ventricular end-diastolic volume index (LVEDVI) at 30 min associated with a lowering of stroke index (SI; p < 0.005 for both), when compared with pre-drug values. In B patients with CI < 3 liter (‘afterload-dependent’ patients) no differences were observed either at 3 min or at 30 min in comparison with values obtained prior to drug administration. Moreover, in this subgroup, like in H patients, there was a negative correlation (p < 0.01) between 3-min percent change of SVRI and 3-min percent change of SI. Our data suggest that in ‘borderline’ hypertension: (a) there may be an increase in peripheral resistance, as in established hypertension, especially when age-matched groups are considered; (b) the earliest sign of compromised left ventricular function is the reduction in dia-stolic PFR but, unlike established hypertension, this index is still correlated with systolic function; (c) cardiac output might be even somewhat reduced and also negatively correlated with vascular resistance (‘afterload-dependent’ hearts); (d) furosemide (acute administration) might contribute to a better definition of hemodynamic behavior.

A reduction of functional capacity has been reported in severe hypertension. However, the reduced peripheral vasodilation observed in the early stages of hypertension, could also impair the blood supply to exercising muscles in mild hypertensives presenting a normal left ventricular mass. In this paper the cardiopulmonary exercise capacity of early hypertensives has been investigated. Thirty mild hypertensives (9 in stage I and 21 in stage II according to WHO) and 36 normotensives divided into two age and weight-matched groups, were investigated. All subjects underwent a stress test according to the modified Bruce protocol with contemporary assessment of breath-by-breath expiratory gas analysis and measurement of the anaerobic threshold (AT) and of the oxygen consumption at peak exercise (PVO2). Exercise duration and maximal workload, in stage I hypertensives, were similar to controls but the O2 consumption was significantly reduced in comparison to controls (P = 0.043). On the contrary, in stage II patients exercise duration, maximal workload, PVO2 and AT were significantly lower than in normotensives. No relationship between myocardial hypertrophy and ergometric or ventilatory (PVO2, AT, VE) parameters was found. In conclusion an early impairment of the aerobic exercise performance is detectable in uncomplicated (stage I WHO) mild hypertensives.

Whether physical training, soon after myocardial infarction (MI), has effects upon intrinsic cardiac function at rest and during exertion remains unresolved. We have evaluated ventricular function using radionuclide angiography at rest and during stress testing before and after 3 months' physical training. This has been correlated with the site of MI and with changes in the ST segment during the maximal exercise test performed before the postmyocardial infarction rehabilitation program. We have studied 27 patients, mean age 54 +/- 10 years, in NYHA class I or II. Twelve showed no changes in the ST segment during erogmetric stress test (group 1); seven showed ST segment depression greater than 1 mm in leads different from those of MI (group 2); eight showed ST segment elevation of 2 mm (group 3). Twelve patients had had anterior MI only (AMI group); twelve inferior MI only (IMI group). After rehabilitation, all patients showed an increased work capacity and a decreased double product at the same work load. In the total group, significant increases were found in the left ventricular ejection fraction (LVEF) and in the contractile regional performance (LVwm) at rest, as well as a lesser decrease in the LVEF during handgrip test. Group 1 showed a significant increase in LVEF, associated with a decrease in left ventricular end-diastolic volume (EDV) at rest. Group 2 showed unchanged variables after rehabilitation. Group 3 showed a better LVEF during handgrip with an increase of EDV at rest. The AMI group showed a better LVEF and LVwm at rest and a better LVEF during handgrip. IMI group showed a better right ventricular ejection fraction during handgrip without improvement in LVEF. No patient with IMI had septal asynergy. We conclude that the effects of rehabilitation were linked to the site of MI and to the functional dynamic status of both ventricles.

An impaired maximal vasodilating capacity has been reported in hypertensives. This study aimed to assess whether mild hypertensives depend on anaerobic metabolism more than do normal subjects during the exercise stress test. The oxygen uptake (VO2) and carbon dioxide output (VCO2) were measured at the anaerobic threshold (AT) and at peak exercise (VO2p and VCO2p) during the cardiopulmonary exercise test by breath-by-breath expiratory gas analysis in 21 mild hypertensives and 19 age-matched normotensives. AT was reached earlier in hypertensives than in normotensives, but with similar VO2 uptake, VCO2 output, and VCO2/VO2 ratio. At peak exercise, however, hypertensives showed lower VO2p than controls (29 +/- 5 v 33 +/- 5 mL VO2/kg/min, (P < .03) but similar VCO2p (36 +/- 6 v 39 +/- 6 mL VCO2/kg/min, P = .19). As a result, the slope of carbon dioxide output increase versus oxygen uptake after anaerobic threshold was steeper in hypertensives than in controls (P < .002). The higher CO2 production per unit of O2 in hypertensives as compared with controls seems to reflect a greater involvement of the anaerobic metabolism to supplement energy output.

The accuracy and reproducibility of a new automatic device (P) specially designed for noninvasive blood pressure monitoring during the exercise stress test were evaluated in 50 consecutive subjects (34 normotensives and 16 hypertensives). Automatic measurements were compared with those taken by a sphygmomanometer (RR). A good agreement between systolic pressure values obtained by the two methods was found (RR 159 +/- 30 mmHg, P 158 +/- 28 mmHg, mean difference = -1.53 +/- 13 mmHg, p = 0.166, ns). On the contrary the new device significantly underestimated diastolic pressure values (RR 89.3 +/- 13 mmHg; P 84 +/- 13 mmHg, mean difference -5.37 +/- 9.3, p < 0.001). In conclusion the new device seems able to measure systolic but underestimates diastolic blood pressure both in hypertensives and in normotensives during the effort test.