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The Cardiovascular Health Study provided the opportunity to determine the association of subclinical and clinical cardiovascular disease with pulmonary function in a population sample of elderly adults. Included were 2,955 women and 2,246 men over age 64 years who were recruited for this observational study from four communities and completed extensive examinations that included spirometry, echocardiograms, and blood pressure. Current smokers, past smokers with >20 pack-years of smoking, and persons with a history of asthma, chronic bronchitis, or emphysema were excluded from this analysis, leaving 2,784 (55%) of the cohort. Systolic hypertension or coronary artery disease was associated with 40- to 100-mL decrements in FEV1, and 50- to 150-mL decrements in FVC, while a history of congestive heart failure was associated with 200 to 300 mL lower FEV1 and FVC values (p < 0.0001), after correcting for age, height, and waist size. Higher left ventricular (LV) mass was also significantly associated with a decrease in FEV1 and FVC in multivariate models. This relationship was strongest with the end-diastolic LV posterior wall thickness component of LV mass. In summary, FEV1 and FVC are reduced in elderly persons with hypertension, ischemic heart disease, higher disease, higher LV mass, and congestive heart failure, though the magnitude of these associations is relatively small unless heart failure supervenes. Substantial decrements in percent predicted FEV1 and FVC should not be attributed to the presence of uncomplicated ischemic heart disease or hypertension alone.

To evaluate the effects of long-standing systemic hypertension on left ventricular (LV) function during daily activities, ambulatory radionuclide monitoring of LV ejection fraction (EF) and blood pressure was performed during exercise and other structured activities in 31 hypertensive patients. Patients were divided into 3 groups based on the absence of LV hypertrophy (group 1 [n = 16], LV mass 107 +/- 12 g/m2), presence of LV hypertrophy without electrocardiographic changes (group 2 [n = 10], LV mass 141 +/- 8 g/m2) and LV hypertrophy with associated electrocardiographic changes (group 3 [n = 5], LV mass 158 +/- 9 g/m2). The groups were similar with respect to age, baseline medication, treated and untreated blood pressure, resting EF and treadmill exercise time. Patients in group 3 had the longest history of hypertension. Peak filling rate was normal in group 1 (2.9 +/- 0.4 end-diastolic volume/s), but reduced at rest in groups 2 (2.4 +/- 0.4) and 3 (2.1 +/- 0.3). Patients in group 1 had normal EF responses to exercise and mental stress testing, as well as during routine ambulatory activities. Patients in group 2 had a blunted EF response to exercise, and those in group 3 had a significantly abnormal response. Both group 2 and 3 patients demonstrated abnormal EF responses to mental stress, as well as cold pressor testing in association with significant increases in mean arterial pressure and marked reduction in diastolic filling rate. Decreases in EF were also observed during routine patient monitoring in 3 group 3 patients and 4 group 2 patients. These events were associated with significantly increased blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular hypertrophy resulting from hypertension is accompanied by significant morbidity and mortality and in advanced stages may be irreversible. Hence, early detection of cardiac changes in hypertensive patients remains an important diagnostic goal. When the hypertrophy is mild or moderate, parameters of left ventricular diastolic function and measurements of left atrial size may facilitate the distinction between normal variation and pathologic increases in left ventricular mass. We measured left ventricular isovolumic relaxation time (IVRT, the time from aortic valve closure to mitral valve opening) and left atrial dimensions and correlated them to left ventricular mass index measured by M-mode echocardiography and rapid left ventricular filling by radionuclide ventriculography. In 20 subjects with untreated mild essential hypertension, IVRT was prolonged compared to a normotensive age-matched control group (91 +/- 23 vs 65 +/- 13 msec, p less than 0.0001). Left atrial dimension index was increased in patients compared to controls (1.9 +/- 0.4 vs 1.4 +/- 0.5 cm/m2, p less than 0.001), and this increase was related to prolonged IVRT (r = 0.46, p less than 0.001). Abnormal IVRT correlated with both increased left ventricular mass and decreased rapid ventricular filling in the hypertensive subjects. Thus, prolonged IVRT and borderline left atrial dimension may help identify subtle pathologic left ventricular mass increases in hypertensive subjects.

To define the extent of left ventricular ejection and filling abnormalities in patients with mild hypertension, a non-imaging nuclear probe was used to generate high resolution time-activity curves in 25 patients with an average systolic blood pressure of 154 +/- 20 mm Hg and diastolic pressure of 98 +/- 8 mm Hg. The hypertensive patients did not meet electrocardiographic criteria for left ventricular hypertrophy, and none had evidence of ischemic or other cardiac disease. Compared with 25 age-matched normal subjects who had average systolic and diastolic pressures of 123 +/- 10 and 79 +/- 8 mm Hg, respectively, the hypertensive patients had a significantly lower ejection rate (2.00 +/- 0.20 versus 2.34 +/- 0.36 end-diastolic counts/s for the control group, p less than 0.05) and ejection fraction (58 +/- 4.9 versus 62 +/- 4.4) (p less than 0.05). The hypertensive patients had a markedly lower average rapid left ventricular filling rate (1.87 +/- 0.32 versus 2.69 +/- 0.41 counts/s for the control group, p less than 0.001). Although there was a modest inverse relation between echocardiographic left ventricular mass index and filling rate in the hypertensive patients (r = -0.59, p less than 0.01), 4 of 12 hypertensive patients with normal left ventricular mass index had a depressed filling rate. All of the hypertensive patients with increased left ventricular mass index had an abnormal left ventricular filling rate (less than 1.89 end-diastolic counts/s).(ABSTRACT TRUNCATED AT 250 WORDS)

Reductions in left ventricular (LV) mass have been reported after antihypertensive therapy with certain sympatholytic agents and converting enzyme inhibitors, but little or no improvement has been noted after vasodilator therapy. In this study we evaluated the effect of the calcium channel blocker nitrendipine on echocardiographic LV mass. During a 12-month period, nitrendipine was used as monotherapy in 30 patients and in combination with propranolol or a diuretic in an additional 28 patients. Nitrendipine monotherapy lowered supine blood pressure from 148/97 to 136/83 mm Hg, but LV mass did not change significantly. Supine blood pressure decreased from 155/103 to 134/86 mm Hg in patients receiving combination therapy but, again, changes in LV mass were not significant. These data suggest that nitrendipine is effective in lowering blood pressure, but this is not associated with a significant decrease in LV mass in patients with mild hypertension.

Abnormal left ventricular diastolic performance, an early manifestation of hypertension in the heart, may precede the development of left ventricular hypertrophy. To assess effects of antihypertensive therapy on the heart, left ventricular mass (determined by echocardiography) and rapid left ventricular filling rate (determined by radionuclide ventriculography) were compared before and after 6 months of treatment of 16 patients. Nitrendipine (a dihydropyridine calcium channel blocker) was given alone or in combination with either propranolol or hydrochlorothiazide, or both, and significantly reduced blood pressure (156/103 +/- 12/7 to 137/89 +/- 10/6 mm Hg). In 6 of the 16 patients, left ventricular mass decreased by more than 10% (270 +/- 95 to 193 +/- 47 g, p less than 0.01); in the same patients, left ventricular filling rate increased (2.03 +/- 0.35 to 2.30 +/- 0.45 end-diastolic counts/s [EDC/s], p less than 0.01). In the one patient whose left ventricular mass increased (137 to 195 g), left ventricular filling rate decreased from 2.01 to 1.78 EDC/s. In the remaining nine patients who had no change in left ventricular mass, there was no significant changes in left ventricular filling. The changes in ventricular mass and filling could not be related to the extent of change in blood pressure or heart rate. These data suggest that regression of left ventricular mass during antihypertensive therapy with nitrendipine is accompanied by improved diastolic function.

To assess the clinical efficacy of chronic nitrendipine therapy in mild to moderate essential hypertension, we studied blood pressure (BP) and heart rate responses in 22 subjects receiving maintenance nitrendipine therapy. Ten subjects (45%) whose hypertension was controlled with chronic monotherapy had an 11/12 mm Hg decrease in supine BP (P less than 0.05) with a mean (+/- SD) dose of 71 +/- 15 mg/day. The 12 (55%) subjects whose hypertension was not controlled with monotherapy had a comparatively higher baseline BP than the other 10 (156/105 +/- 10/6 compared with 150/98 +/- 15/4 mm Hg; P less than 0.05). Eight of the 10 subjects demonstrating office BP control with chronic nitrendipine monotherapy who also had full-time employment underwent continuous ambulatory BP monitoring before and after maintenance monotherapy. Nitrendipine induced a reduction in the mean 24-hour BP and mean BP at home, but did not reduce the BP during work or while asleep. These data suggest that nitrendipine lowers BP when assessed by casual office methods. The ambulatory BP monitor data demonstrate that the hypotensive response to chronic nitrendipine is modified during work periods, which are generally associated with increased adrenergic activity. Ambulatory BP monitoring may be superior to office (casual) monitoring in the assessment of the overall efficacy of antihypertensive drugs.

Left ventricular hypertrophy is associated with abnormal left ventricular diastolic filling in patients with hypertension. To assess the effects of antihypertensive therapy on the heart in nine previously untreated patients with echocardiographically-detected left ventricular hypertrophy, left ventricular mass and rapid left ventricular filling rate were compared before and after 6 months of treatment with metoprolol monotherapy. Metoprolol was given in doses of 100 to 400 mg/day (average dose, 167 mg/day in two divided doses) and significantly reduced both casual, office blood pressure (150/101 to 130/86 mm Hg, p less than 0.01) and 24-hour ambulatory blood pressure (139/91 to 126/79 mm Hg, p less than 0.05 for systolic, p less than 0.01 for diastolic). Following treatment with metoprolol, left ventricular mass index decreased from 135 +/- 20 to 120 +/- 13 gm/m2 (p less than 0.05), while rapid left ventricular filling rate increased from 1.89 +/- 0.24 to 2.09 +/- 0.27 end-diastolic volumes/sec (p less than 0.01). The reduction in left ventricular mass index was secondary to decreased posterior and septal wall thicknesses (13% and 11%, respectively, p less than 0.05 for both), as there were no changes in the left ventricular internal dimensions. Neither resting nor exercise left ventricular ejection fraction changed on metoprolol therapy compared to the baseline values. These data demonstrate that regression of left ventricular hypertrophy in never-previously-treated hypertensive patients is accompanied by improved diastolic performance following beta-adrenergic blocker monotherapy.