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Left ventricular mass, fractional shortening, and end systolic wall stress (mechanical indices) measured by echocardiography and the response of fractional shortening and end systolic wall stress to the infusion of isoproterenol (0.02 microgram/kg/min for 5 min) (a non-mechanical index) were studied in 57 patients (mean (SD) age 49(8)) with essential hypertension. Nineteen patients had subnormal end systolic wall stress (group 1), 25 patients had normal end systolic wall stress and slightly increased left ventricular mass (group 2A), and 13 patients had normal end systolic wall stress and considerably increased left ventricular mass (group 2B). Plasma noradrenaline concentration was higher in group 2B than in the other groups. When end systolic wall stress was greater than 12 g/cm2 this variable showed a significant inverse linear relation with fractional shortening before isoproterenol infusion. The inotropic response to isoproterenol was measured as the increase of fractional shortening corrected for the decrease of end systolic wall stress (delta fractional shortening/--delta end systolic wall stress). The mean (SD) change in delta fractional shortening/--delta end systolic wall stress was significantly larger in group 1 (1.40 (0.60) cm2/g) than in group 2A (0.85 (0.39) cm2/g), and was significantly larger in group 2A than in group 2B (0.56 (0.15) cm2/g). In patients with hypertensive hypertrophy with subnormal end systolic wall stress (inappropriate hypertrophy) the beta adrenergic response is increased; in hypertensive hypertrophy with normal end systolic wall stress (appropriate hypertrophy), however, it is normal, or becomes reduced as plasma noradrenaline increases. [ABSTRACT FROM PUBLISHER]

Objective: The objective of this study is to evaluate the efficacy and safety of sacubitril/valsartan (LCZ696, an angiotensin receptor and neprilysin inhibitor) add-on to amlodipine compared with amlodipine monotherapy in Asian patients with systolic hypertension uncontrolled with amlodipine., Methods: Patients with mean clinic SBP at least 145 mmHg and less than 180 mmHg after a 4-week treatment with amlodipine 5 mg/day were randomized to receive LCZ696/amlodipine (200/5 mg/day) or amlodipine 5 mg/day for 8 weeks. The primary assessment was the superiority of LCZ696/amlodipine versus amlodipine in lowering 24-h ambulatory SBP from baseline to week 8. Secondary assessments included 24-h ambulatory DBP and pulse pressure (PP), daytime and night-time BP, clinic BP and PP, BP control/responder rate (<140/90 mmHg or a reduction ≥20/10 mmHg from baseline), and safety., Results: Of the 371 patients screened, 266 (71.7%) patients (mean age 55.4 years; 24-h SBP/DBP 139.0/86.1 mmHg at baseline) who did not respond to 4-week treatment with amlodipine 5 mg/day were randomized. At week 8, LCZ696/amlodipine provided greater reductions in 24-h SBP compared with amlodipine monotherapy from baseline (-13.9 versus -0.8 mmHg, P < 0.001). All the secondary efficacy assessments were significantly (P < 0.001) in favour of LCZ696/amlodipine, for instance, 24-h PP (-5.8 versus -0.6 mmHg). Overall, the incidence of adverse events was 20.0% with LCZ696/amlodipine and 21.3% with amlodipine., Conclusion: LCZ696/amlodipine showed significantly greater 24-h ambulatory BP and PP reductions compared with amlodipine monotherapy. Both treatments were generally well tolerated. Therefore, LCZ696/amlodipine combination could be an effective treatment for patients with systolic hypertension uncontrolled with amlodipine.

Objective: To investigate the relationship between cervical lesions and patient age, brushing method and bruxism based on a clinical survey of first-appointment patients., Methods: Two hundred and nine patients (118 male, 91 female) who had unfilled cervical lesions were examined. Information on patient age, teeth with lesions, classification of the lesions, brushing method and bruxism was obtained. The data were analysed statistically., Results: Cervical lesions started to develop in the first premolar teeth in the early twenties and became more prevalent with age. A habit of bruxism was associated with an increase in cervical lesions. Brushing was not directly associated with the development of cervical lesions., Conclusion: This study suggests that cervical lesions should be treated at an early stage to prevent further problems.

Objectives: We sought to assess whether isoproterenol stress echocardiography could detect in advance in which patients hypertrophic cardiomyopathy would progress to a phase resembling dilated cardiomyopathy., Background: In a few patients, hypertrophic cardiomyopathy has been reported to progress to a phase characterized by systolic dysfunction and left ventricular dilation, resembling dilated cardiomyopathy., Methods: Echocardiograms were recorded before and immediately after intravenous infusion of isoproterenol (0.02 microgram/kg body weight per min) for 5 min in 18 patients with typical hypertrophic cardiomyopathy (i.e., hypertrophied, hyperdynamic and nondilated) to determine the difference in fractional shortening. The patients were categorized into those with a good response (difference in fractional shortening > 7%, 14 patients) and those with a poor response (difference < or = 7%, 4 patients). Changes in left ventricular end-diastolic diameter and fractional shortening were evaluated by using serial echocardiography over an average follow-up period of 5.4 years., Results: In the good response group, neither end-diastolic diameter nor fractional shortening changed significantly during the follow-up period. In the poor response group, end-diastolic diameter significantly increased from a mean +/- SD of 41 +/- 5 to 53 +/- 5 mm (p < 0.05), and fractional shortening significantly decreased from 40 +/- 12% to 29 +/- 10% (p < 0.05). All patients in the poor response group showed a substantial decrease (> or = 5%) in fractional shortening and an increase (> or = 5 mm) in end-diastolic diameter. One patient developed congestive heart failure due to systolic dysfunction during the observation period., Conclusions: The present study confirmed that impaired responses to isoproterenol infusion are related to future deterioration of left ventricular performance in patients with typical hypertrophic cardiomyopathy.

Sixteen patients with dilated cardiomyopathy were studied to define the abnormality of the beta-adrenergic pathway non-invasively, using echocardiographic left ventricular responses to isoproterenol (ISP; 0.02 microgram/kg/min) and dibutyryl cyclic AMP (DBcAMP; 0.1 mg/kg/min) infusion. The increase in fractional shortening induced by ISP (delta FS-ISP) was 9 +/- 6% and that by DBcAMP (delta FS-DBcAMP) was 7 +/- 3%. The patients could be divided into three groups according to their left ventricular response to each agent: Group A; normal response to ISP (delta FS-ISP > or = 11%), Group B-1; poor response to ISP but better response to DBcAMP (delta FS-ISP < 11%, delta FS-DBcAMP > or = 7%; damage to beta-receptors), and Group B-2; poor response to ISP and DBcAMP (delta FS-ISP < 11%, delta FS-DBcAMP < 7%; damage including post receptor levels). Seven patients were in Group A, four in Group B-1, and five in Group B-2. DCM patients had a diversity of left ventricular responses to ISP and DBcAMP, according to the site of damage in the beta-adrenergic pathway.

To analyze the adrenergic responses and to compare them between hypertensive patients with and without left ventricular hypertrophy (LVH), left ventricular (LV) fractional shortening (FS) and end-systolic wall stress (ESS) were measured by echocardiography and the inotropic response to the infusion of isoproterenol (0.02 micrograms/kg/min for 5 min) was studied in 25 hypertensive patients without LVH [H(-)] and 30 hypertensive patients with LVH [H(+)]. LVH was determined by echocardiography. Age, gender, heart rate, systolic and diastolic blood pressures, LV end-systolic and end-diastolic diameters, and FS were matched between the groups. The tests were performed before introduction of antihypertensive treatment or 4 weeks after its discontinuation. ESS showed a significant inverse linear relation with FS in all the subjects before isoproterenol infusion. The inotropic response to isoproterenol was measured as the increase of FS corrected for the decrease of ESS (delta FS/-delta ESS), that is, the slope of the change of the relation between FS and ESS. The change in delta FS/-delta ESS was significantly smaller (0.49 +/- 0.15 cm2/g, mean +/- SD) in H(-) than in H(+) patients (1.01 +/- 0.57 cm2/g) (p < 0.001). It is concluded that, compared with the H(+) group, adrenergic response is depressed in H(-) patients. This depression might be etiologically related to the phenomenon that LVH did not develop in the H(-) group in spite of the same level of pressure load as in the H(+) group.

To investigate the clinical roles of mechanical and non-mechanical factors in hypertensive hypertrophy, 125 patients with essential hypertension, 20 with hypertrophic cardiomyopathy (HCM) and 20 with dilated cardiomyopathy (DCM), were studied using echocardiography. The hypertensive patients were separated into 3 groups: those with left ventricular (LV) hypertrophy (H), those without hypertrophy (H(-)) and those with dilatation (D). Group H patients were separated into 3 subgroups: those with subnormal LV end-systolic wall stress (ESS) (HI), those with normal ESS and mild hypertrophy (HIIA), and those with normal ESS and severe hypertrophy (HIIB). The inotropic response to isoproterenol infusion (0.02 microgram/kg/min for 5 min) was measured by the increase of fractional shortening (FS) corrected for the decrease of ESS (delta FS/delta ESS). After antihypertensive treatment for 4.4 +/- 1.7 years, echocardiography was repeated. delta FS/delta ESS was significantly larger in HI and HCM than in HIIA, was significantly larger in HIIA than in HIIB in which it was significantly larger than in D and DCM. After the treatment, LV mass decreased significantly except in HI. In conclusion, hypertensive hearts are regulated by mechanical and non-mechanical factors. Non-mechanical factors, for example the function of beta-adrenergic receptors in myocardium, have a variety of influences on myocardium, causing a broad spectrum of clinical features and courses.

To study the cardiac determinants of regression of left ventricular hypertrophy in hypertension, left ventricular mass, fractional shortening and end-systolic wall stress were measured echocardiographically in 36 patients with essential hypertension and left ventricular hypertrophy. The patients were classified into two groups. Group I consisted of 15 patients with subnormal end-systolic wall stress, and Group II consisted of 21 patients with normal end-systolic wall stress. There were no significant differences between groups in systolic or diastolic blood pressure. After treatment for 4.4 +/- 1.7 years, echocardiographic studies were repeated. There were no significant differences between groups in the duration of the follow-up period and the kinds of antihypertensive drugs. After treatment, blood pressure decreased significantly in both groups (p less than 0.001 for both), with no significant difference between groups. Left ventricular mass increased significantly in Group I (from 331 +/- 7 to 363 +/- 24 g, mean +/- SEM, p less than 0.05), whereas it decreased significantly in Group II (from 318 +/- 16 to 268 +/- 17 g, p less than 0.001). Myocardial contractility (the relation between end-systolic wall stress and fractional shortening) remained almost the same as before treatment. In conclusion, in patients with hypertensive ventricular hypertrophy with subnormal end-systolic wall stress (inappropriate hypertrophy, probably induced by a neurohumoral factor), a decrease in blood pressure with antihypertensive treatment does not lead to regression of left ventricular hypertrophy, but rather to an increase in left ventricular mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertensive cardiac hypertrophy of 20 patients was classified as inappropriate hypertrophy (HH-I) and appropriate hypertrophy (HH-II) according to their end-systolic wall stress, as measured by echocardiography. The differences in systolic and diastolic performances among the HH-I and HH-II subjects and 10 normal controls (NC) before and during isoproterenol infusion were investigated. Eight patients had subnormal end-systolic wall stress (inappropriate hypertrophy) and 12, normal end-systolic wall stress (appropriate hypertrophy). Before isoproterenol infusion, normalized peak rate of a change in left ventricular diameter during systole was significantly greater in HH-I (3.5 +/- 0.8/s) than in NC (2.3 +/- 0.5/s) and HH-II (2.6 +/- 0.6/s) (p less than 0.01 and p less than 0.005), but there was no significant difference between HH-II and NC. There was no significant difference in normalized peak rate of a change of left ventricular diameter during the rapid filling phase among the three groups (4.5 +/- 1.2/s in HH-I, 4.0 +/- 1.6/s in HH-II, and 4.2 +/- 0.8/s in NC). During isoproterenol infusion, normalized peak rate of a change of left ventricular diameter during systole was significantly greater in HH-I (7.0 +/- 1.9/s) than in HH-II (4.8 +/- 1.7/s) and NC (4.8 +/- 0.8/s) (p less than 0.05 and p less than 0.01, respectively), but there was no significant difference between HH-II and NC. Normalized peak rate of a change of left ventricular diameter during rapid filling was significantly less in HH-II (4.8 +/- 1.7/s) than in HH-I (7.3 +/- 1.3/s) and NC (6.5 +/- 0.8/s) (p less than 0.005 and p less than 0.005, respectively), but there was no significant difference between HH-I and NC. These results suggest that hypertensive patients with inappropriate hypertrophy have relatively diminished diastolic velocity (supernormal systolic velocity and normal diastolic velocity) before and during isoproterenol infusion, and that hypertensive patients with appropriate hypertrophy have absolutely diminished diastolic velocity during isoproterenol infusion, in spite of normal diastolic velocity before the infusion.

The clinical features of 20 patients with mildly dilated cardiomyopathy (MDCM) were investigated by electrocardiography and echocardiography. MDCM was defined as conditions with: 1) left ventricular end-diastolic dimension between 55 and 65 mm and 2) left ventricular fractional shortening between 10 and 25%. Nine patients (45%) had no histories of congestive heart failure. Eight patients had atrial fibrillation, and the other 12 patients were in regular sinus rhythm. Two patients had supraventricular premature contractions and five patients had ventricular premature contractions. One patient had paroxysmal atrial tachycardia. During the 40-months' span of this echocardiographic study, left ventricular end-diastolic dimension (60.8 +/- 3.8 mm to 57.3 +/- 4.6 mm) and left ventricular fractional shortening (17.2 +/- 4.6% to 22.7 +/- 7.1%) did not change significantly. One patient died suddenly. These results suggest that 1) some patients with MDCM have neither definite histories nor symptoms to suggest heart failure; 2) the hemodynamic conditions of patients with MDCM do not always deteriorate, but rather stabilize, and even improve during follow-up periods; 3) several types of arrhythmias can be observed, even in standard resting electrocardiograms; and 4) patients with MDCM may die suddenly.

Pre-operative and post-operative echocardiographic data were analyzed from 8 patients with acromegaly. Pre-operatively, end-diastolic diameter was greater than 55 mm in 5 patients (63%) and concentric left ventricular hypertrophy was observed in 3 patients (38%). However, left ventricular function was normal (fractional shortening of the left ventricle greater than 28%) in all patients except 1. All patients had increased left ventricular mass. There was no significant correlation between left ventricular mass and basal plasma growth hormone concentration. An average of 23.9 months after hypophysectomy, growth hormone concentration was significantly decreased. However, the abnormal echocardiographic findings remained. In conclusion, echocardiographic abnormalities (left ventricular dilatation and hypertrophy) are common in patients with acromegaly, but systolic function is, in general, maintained. These cardiac abnormalities persist after reduction of plasma growth hormone concentration.

Quantitative assessment of left ventricular function in patients with coronary artery disease was made by computer analysis of two-dimensional echocardiography performed during a cold pressor test. Short-axis cross-sectional images of the left ventricle at the levels of the mitral valve and chordae tendineae were recorded by a phase array sector scanner in 12 patients with coronary artery disease and 11 normal controls. Endocardial outlines at end-diastole and end-systole were traced and analyzed by a computer system. The short-axis cross-sectional images were divided into octants and were analyzed. The segmental area and its changes during the cardiac cycle were measured and calculated for each octant. Regional function of the left ventricle was evaluated by percent changes of segmental area. The regional segmental area changes in patients with coronary artery disease were compared with those in normal controls. Similar increments were achieved in rate pressure product in the 2 groups. In relation to the perfusing coronary arteries, 8 segments were integrated arbitrarily into 3 walls (anteroseptal wall, lateral wall, and posterior wall and posterior septum). The cold pressor test induced wall motion abnormalities in 12 of 16 walls which were supplied by stenosed coronary arteries. In contrast, wall motion abnormalities were detected in only 5 of 38 walls which were supplied by coronary arteries without significant stenotic lesions. The sensitivity of cold pressor test-induced wall motion abnormalities in detecting coronary artery disease was 75% and the specificity was 87%. No serious complications were encountered in this study. In conclusion, computer-aided cold pressor two-dimensional echocardiography is a safe and sensitive method for the assessment of left ventricular function and diagnosis of coronary artery disease.

A 67-year-old man with a sigmoid septum causing the left ventricular outflow obstruction by inotropic stimulation was reported. This patient was admitted to the Hospital of the University of Tsukuba because of chest pain. Phonocardiography revealed a systolic ejection murmur which was intensified by amyl nitrite inhalation. A carotid pulse tracing showed a mid-systolic dip and a secondary slow wave during amyl nitrite inhalation. M-mode echocardiography demonstrated neither systolic anterior motion of the mitral valve (SAM) nor mid-systolic closure of the aortic valve at rest. Two-dimensional echocardiography revealed a basal interventricular septum markedly protruding into the left ventricle (sigmoid septum). The remainder of the septum and the left ventricular free wall were not hypertrophied, and no enlargement of the left ventricular cavity was observed. During exercise tests, blood pressure dropped significantly. Cardiac catheterization showed a pressure gradient within the left ventricle with isoproterenol infusion and post-extrasystolic potentiation. These findings suggest that left ventricular outflow tract obstruction could occur in a patient with sigmoid septum by inotropic stimulation, producing a fall of blood pressure during exercise.

The comparative sensitivities of exercise (supine ergometer), isoproterenol (ISP) infusion and cold pressor test (CPT) for detecting myocardial ischemia in patients with effort angina (45 cases) and vasospastic angina (16 cases) were investigated. Twenty-three patients with atypical chest pain served as normal controls. Left ventricular function was evaluated by computerized quantitative analysis using the following three graphic methods: 1) radionuclide angiography during exercise (EX-RI) and ISP infusion (ISP-RI), 2) two-dimensional echocardiography during ISP infusion (ISP-2DE) and CPT (CP-2DE) and 3) digital subtraction angiography during CPT (CP-DSA). The incidence of regional wall motion abnormalities (WMA) induced by these three stress tests in patients with effort angina were as follows: 83% in EX-RI, 80% in ISP-2DE, 80% in ISP-RI, 75% in CP-2DE and 86% in CP-DSA. In patients with vasospatic angina, the WMA were as follows: 40% in EX-RI, 0% in ISP-RI and 71% in CP-DSA. In patients with atypical chest pain, the WMA were 0% in EX-RI, 0% in ISP-RI, 8% in ISP-2DE, 13% in CP-2DE and 13% in CP-DSA. The left ventricular ejection fraction (EF) was unchanged during ISP (from 65 +/- 11% to 68 +/- 12%) and it decreased both during exercise (from 64 +/- 10% to 58 +/- 9%, p less than 0.05) and during CPT (from 69 +/- 10% to 65 +/- 9%, p less than 0.05) in patients with effort angina. In patients with vasospastic angina, the EF was unchanged both during exercise (from 70 +/- 7% to 68 +/- 13%) and during the CPT (from 76 +/- 5% to 75 +/- 4%), while it increased during ISP infusion (from 63 +/- 8% to 79 +/- 7%, p less than 0.01). In patients with atypical chest pain, the EF was increased both during exercise (from 72 +/- 7% to 79 +/- 5%, p less than 0.01) and during ISP infusion (from 67 +/- 5% to 78 +/- 7%, p less than 0.01), while it was unchanged during CPT (from 77 +/- 7% to 76 +/- 8%). In exercise and in ISP infusion tests, WMA were provoked concomitantly with ST segment deviations in nearly all patients. However, during CPT, WMA were produced without the occurrence of ST segment deviations. Myocardial ischemia due to organic coronary artery stenosis was difficult to distinguish from coronary artery spasm by exercise test. However, the susceptibility to ISP infusion and CPT differed in producing WMA in patients with vasospastic angina.(ABSTRACT TRUNCATED AT 400 WORDS)

To evaluate the prognostic value of the left ventricular response to isoproterenol infusion in patients with dilated cardiomyopathy (DCM), 25 patients, 17 men and eight women, were studied. According to responses of left ventricular function to isoproterenol (0.02 microgram/kg/min), the patients were classified in two groups: the normal response group, in which fractional shortening increased by more than 10% (n = 10); and the low response group, in which fractional shortening increased by 10% or less (n = 15). A follow-up spanning four to 40 months with an average of 21 months disclosed that six patients died, two deteriorated, and six had no change in the low response group, while seven patients were improved, three stabilized, and no one deteriorated or died in the normal response group. There was a difference in the clinical courses of the two groups. Thus, the left ventricular response to isoproterenol proved useful in predicting the course of DCM.