Left ventricular remodeling in patients with metabolic syndrome: influence of gender.

AIM: The study was aimed to evaluate the influence of gender on left ventricular (LV) remodeling in metabolic syndrome (MetS). METHODS AND RESULTS: We enrolled 200 subjects without diabetes or overt cardiovascular diseases, never treated with anti-hypertensive drugs or statins: 60 men and 40 women with MetS matched by age, gender and 24 h systolic and diastolic blood pressure (BP) with 60 men and 40 women without MetS. The patients underwent blood tests, 24 h our BP monitoring, LV echocardiographic examination. LV mass indexed by eight(2.7) was significantly greater in men and women with MetS than without MetS. Compared with women without MetS, women with MetS had significantly higher posterior wall thickness and relative wall thickness, greater prevalence of LV concentric remodeling/hypertrophy and lower indices of LV diastolic function, whereas all these parameters were not significantly different between men with and without MetS. MetS was an independent predictor of relative wall thickness and LV mass index in women, but not in men. CONCLUSION: The impact of MetS on LV remodeling is significantly influenced by gender: the effects of MetS are more pronounced in women, with development of LV concentric hypertrophy/remodeling and preclinical diastolic dysfunction.

Intracranial bleeding risk after minor traumatic brain injury in patients on antithrombotic drugs.

BACKGROUND: Intracranial haemorrhage (ICH) risk after minor traumatic brain injury (mTBI) in patients on antithrombotic treatment is unclear. We compared ICH rates in mTBI patients on single, double and no antithrombotic therapy. Antithrombotic drugs encompassed vitamin K antagonists (VKAs), direct oral anticoagulants (DOACs) and antiplatelets. Secondary aim was to identify potential predictors of ICH. METHODS: We retrospectively analysed consecutive adults referred to our emergency department for mTBI. All clinical information was retrieved by patients' charts review. Patients were divided in 5 groups: 1) no antithrombotic users, 2) antiplatelet users, 3) vitamin K antagonist users, 4) direct oral anticoagulants users, and 5) double antithrombotic users. RESULTS: A total of 1846 patients were enrolled, mean age 71 years (IQR 46-83); 1222 (66.2%) were in group 1, 407 (22.0%) in group 2, 120 (6.5%) in group 3, 51 (2.7%) in group 4 and 46 (2.5%) in group 5. At entry, 1387 (75.1%) patients underwent brain CT, 787 (64.4%) in group 1, 387 (95.1%) in group 2, 119 (99.2%) in group 3 and 51 (100%) in group 4 and 43 (93.5%) in group 5. ICH was documented in 36 patients (4.6%; CI 95%: 3.2-6.3) in group 1, 22 (5.9%; CI 95%: 3.6-8.5) in group 2, 5 (4.2%; CI 95%: 1.4-9.5) in group 3, 2 (3.9%; CI 95%: 0.5-13.5) in group 4 and 3 (7.0%; CI 95%: 1.5-19.1) in group 5 (p-value for across groups comparison = 0.86). At multivariable analysis GCS < 15 (OR 7.95 CI 95%: 3.12-20.28), post-traumatic amnesia (OR 6.49; CI 95%:3.57-11.82), vomiting (OR 4.45 CI 95%:1.47-13.50), clinical signs of cranial fractures (OR 8.41 CI 95%: 2.12-33.33), scalp lesions (OR 2.31 CI 95%: 1.09-4.89), but none of antithrombotic drugs were independently associated with ICH. CONCLUSION: mTBI-related ICH rate was similar in patients with and without antithrombotic use. Potential predictors of ICH can be drawn from patients' clinical examination.

Endogenous beta-endorphins in hypertension: correlation with 24-hour ambulatory blood pressure.

OBJECTIVES: The aims of this study were to determine whether hypertensive patients showed increased endogenous opioid tone and to find a possible correlation between beta-endorphin levels and 24-h ambulatory blood pressure. We also investigated whether circulating beta-endorphin levels were associated with pain perception at rest. BACKGROUND: Experimental studies suggest an involvement of the endogenous opioid system in cardiovascular control mechanisms. METHODS: We determined baseline beta-endorphin plasma levels by radioimmunoassay in 81 consecutive subjects (48 hypertensive, 33 normotensive) after a 30-min rest and before 24-h ambulatory blood pressure monitoring. In 72 of 81 subjects with a dental formula suitable for the pulpar test (graded increase of test current -0 to 0.03 mA applied to three healthy teeth), pain perception was also investigated. RESULTS: Hypertensive patients showed higher beta-endorphin plasma levels than normotensive subjects (p < 0.002). Circulating endogenous opioid levels correlated with 24-h diastolic blood pressure (p < 0.01), whereas the relation with systolic pressure did not reach statistical significance. When 24-h blood pressure recordings were divided into daytime and nighttime values, and blood pressure loads (percent of measurements > or = 140 mm Hg for systolic blood pressure and > or = 90 mm Hg for diastolic pressure) were calculated, a significant correlation was found between beta-endorphin levels and diastolic pressures and load. Similarly, presampling diastolic blood pressure was significantly correlated with beta-endorphin levels. Of the 72 subjects tested, hypertensive patients showed a lower pain sensitivity than normotensive subjects. A positive correlation was found between pain threshold and circulating beta-endorphin levels (p < 0.05). CONCLUSIONS: Sustained arterial pressure is probably involved in the tonic activation of cardiovascular mechanisms linked to endogenous opioid tone. Circulating plasma endorphins may account, at least in part, for the pain perception pattern relating to blood pressure levels at rest.

Left ventricular changes in isolated office hypertension: a blood pressure-matched comparison with normotension and sustained hypertension.

BACKGROUND: Isolated office (IO) hypertension is a benign condition according to some researchers, whereas others believe it is associated with cardiovascular abnormalities and increased cardiovascular risk. The aim of this study is to compare morphofunctional characteristics of the left ventricle (LV) in IO hypertensive subjects, normotensive subjects (hereafter, hypertensives and normotensives), and never-treated sustained hypertensives. The 3 groups were matched not only by age, sex, and body mass index but also by clinic blood pressure (BP) (IO hypertensives and sustained hypertensives) and daytime BP (IO hypertensives and normotensives). METHODS: We enrolled 42 IO hypertensives (clinic BP > 140 and/or 90 mm Hg and daytime BP < or = 130/80 mm Hg), 42 sustained hypertensives (clinic BP > 140 and/or 90 mm Hg and daytime BP > or = 140 and/or 90 mm Hg) and 42 normotensives (clinic BP < 135 and/or 85 mm Hg and daytime BP < or = 130/80 mm Hg). Left ventricular morphologic features and function were assessed using digitized M-mode echocardiography. RESULTS: Compared with normotensives, IO hypertensives had significantly thicker LV walls, increased LV mass, reduced diastolic function, increased prevalence of LV hypertrophy, and preclinical diastolic dysfunction. Sustained hypertensives, compared with IO hypertensives, had significantly thicker LV wall, higher LV mass, and lower diastolic function, whereas the prevalence of LV hypertrophy and preclinical diastolic dysfunction was greater than in IO hypertensives, but the difference did not reach statistical significance (P = .29). CONCLUSIONS: Comparing matched BP groups, IO hypertensives have LV morphofunctional characteristics considerably different from normotensives and qualitatively similar to sustained hypertensives. Therefore, our results support the hypothesis that IO hypertension should not be considered as simply a benign condition.

Longitudinal changes of insulin sensitivity in essential hypertension: influence of blood pressure control and familial predisposition to hypertension.

The aim of this study was to evaluate the influence of blood pressure (BP) control and familial predisposition to hypertension on longitudinal changes in insulin sensitivity in essential hypertension. We evaluated 6 groups of subjects twice (basal: before any treatment; 2nd: after at least 18 months): 42 hypertensives (H) with a family history of hypertension (F+) and 30 H without a family history of hypertension (F-) successfully treated with angiotensin-converting enzyme inhibitors and/or calcium channel blockers (2nd: 24-h BP < or = 130/80 mm Hg); 22 untreated (UT) HF+ and 18 UTHF- (2nd: 24-h BP >140 and/or 90 mm Hg); 18 normotensives F+ and 15 normotensives F-. The parameters evaluated were as follows: glucose, insulin, and C-peptide (Cp) response to an oral glucose load. Glucose was normal in all of the subjects, similar among the 6 groups, and unchanged at the 2nd evaluation. At the basal evaluation insulin and Cp were higher and the metabolic clearance rate (MCR) of glucose was lower in the three F+ groups compared with the corresponding F- groups. In the 2nd evaluation insulin and Cp were reduced and the MCR of glucose increased in THF-, whereas all metabolic parameters were unchanged in THF+; in both UT hypertensive groups insulin and Cp increased and the MCR of glucose decreased, more so in F+ than in F-; in normotensive groups metabolic parameters did not change. A familial predisposition to hypertension influences insulin sensitivity changes during successful antihypertensive therapy, with an improvement in insulin sensitivity in F- and no changes in F+. A persistently high BP has a negative influence on insulin sensitivity in F+ and F-; this influence is greater when high BP is associated with a familial predisposition to hypertension.

Treatment with enalapril modifies the pain perception pattern in hypertensive patients.

The cardiovascular system shares numerous anatomic and functional pathways with the antinociceptive network. The aim of this study was to investigate whether angiotensin-converting enzyme (ACE) inhibitor treatment could affect hypertension-related hypalgesia. Twenty-five untreated hypertensive patients, together with a control group of 14 normotensive subjects, underwent dental pain perception evaluation by means of a pulpar test (graded increase of test current applied to healthy teeth). After the evaluation of the dental pain threshold (occurrence of pulp sensation) and tolerance (time when the subjects asked for the test to be stopped), all the subjects underwent a 24-hour ambulatory blood pressure monitoring. The hypertensive group then was treated with 20 mg/d enalapril, whereas the normotensive subjects remained without any treatment. After a time interval of 6+/-2 months, the dental pain sensitivity was retested in all the subjects, and ambulatory blood pressure was recorded during treatment in the hypertensive patients. At the first assessment, hypertensive patients showed a higher pain threshold than normotensive subjects (P<.001). On retesting of pain sensitivity in hypertensive patients, a significant decrease of both pain threshold and tolerance, leading to their normalization, was observed during treatment (P<.001 and P<.005, respectively), in the presence of reduced 24-hour and office blood pressure values. A slight, though significant, correlation was observed between variations in pain tolerance and baseline blood pressure changes occurring during treatment. During follow-up, the normotensive subjects did not show any significant pain perception or office blood pressure changes. Hypertension-related hypalgesia was confirmed. Mechanisms acting both through lowering of blood pressure and specific pharmacodynamic properties may account for the normalization of pain sensitivity observed in hypertensive patients during treatment with ACE inhibitors.

Twenty-four-hour noninvasive blood pressure monitoring and pain perception.

Although a hypertension-related hypalgesia has been described, the relation between pain perception and the 24-hour blood pressure trend is still unknown. The ambulatory blood pressure monitoring parameters and dental pain sensitivity were correlated in 67 male subjects. The pulpar test (graded increase of test current of 0 to 0.03 mA) was performed on three healthy teeth, and mean dental pain threshold (occurrence of pulp sensation) and pain tolerance (time when the subjects asked for the test to be stopped) were evaluated. Three groups of subjects with normal (n = 34), intermediate (n = 13), and high (n = 20) blood pressure values were identified according to ambulatory monitoring results. Pain threshold differed among the three groups (P < .02), being higher in the group with highest blood pressure. The groups of hypertensive subjects showed higher pain tolerance than the normotensive group (P < .02). Pain threshold was correlated with 24-hour, diurnal, and nocturnal blood pressure values. Pain tolerance was also related to 24-hour blood pressure and to diurnal and nocturnal diastolic and mean arterial pressure values. Systolic and diastolic blood pressure loads were significantly associated with pain threshold, and diastolic load was also associated with tolerance. The blood pressure variability (SD) did not relate to pain perception. The 24-hour arterial pressure was more closely associated with pain perception than the blood pressure values obtained before the pulpar test. A close correlation between pain perception and 24-hour ambulatory blood pressure was demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of arithmetic mental stress test on hypertension-related hypalgesia.

AIM: Though hypertension-related hypalgesia has been described, little is known about possible variation of pain perception after mental stress. The aims of the present study were to determine (1) whether mental stress can influence pain perception in normotensive and hypertensive subjects and (2) whether blood pressure levels before pain evaluation can account for changes in pain sensitivity. PATIENTS AND METHODS: A pulpar test (graded increase in test current of 0-0.03 mA applied on healthy teeth) was performed twice (time interval 15 min) in 62 subjects. Thirty-eight subjects (group 1) performed an arithmetic mental stress test immediately after the first pulpar test while 24 subjects (group 2) did not. The pain threshold (occurrence of pulp sensation) was evaluated as the mean value of three teeth tested on each subject and as the value on the most sensitive tooth. RESULTS: Twenty-eight subjects with normal 24-h blood pressure showed a lower mean pain threshold than 34 subjects with high 24-h blood pressure values (P<0.02). In group 1 (20 normotensives, 18 hypertensives), even when the mental stress increased the pretest blood pressure, the pressure values immediately before both pulpar tests remained similar. In the second pulpar test, a significant increase in the pain threshold on the most sensitive tooth was observed in group 1 (P<0.005). Though a trend towards an increase in the pain threshold was found in both the subgroups of normotensive and hypertensive subjects, the difference was significant in hypertensives only. However, group 2 subjects showed unchanged pain sensitivity on the second test. CONCLUSIONS: A mental stress-induced reduction in pain sensitivity was observed in the absence of change in arterial pressure measured immediately before pulpar tests. A blood pressure increase during the test and, more likely, cortical and humoral activation during stress, may account for the variation found in pain perception.

Relationship between dental pain perception and 24 hour ambulatory blood pressure: a study on 181 subjects.

OBJECTIVE: To investigate dental pain perception in a large group of essential hypertensive subjects. METHODS: A total of 130 hypertensive patients together with 51 normotensive subjects were submitted to tooth-electrical stimulation to determine the dental pain threshold (occurrence of pulp sensation) and tolerance (time when the subject asked for the test to be stopped). Blood pressure was measured at rest, before pain perception evaluation, and during a 24 h period by ambulatory monitoring. RESULTS: The normotensive and hypertensive subjects differed with regard to pain threshold (P = 0.002) and tolerance (P = 0.01). Pain perception variables were significantly correlated with both resting blood pressure and 24 h, diurnal and nocturnal arterial pressures, the correlation between pain threshold and 24 h systolic blood pressure being the most significant (r = 0.31, P < 0.0001). By contrast, parameters indicating 24 h blood pressure variability (percentage of nocturnal blood pressure reduction and 24 h blood pressure variation coefficients) were not associated with pain perception. Moreover, among the hypertensives only, a significant relationship was observed between pain sensitivity and both baseline and 24 h pressures. No association was found when pain perception and blood pressure were correlated in the normotensive group. CONCLUSIONS: The correlation between both baseline and 24 h blood pressure and pain perception has been confirmed in a large group study of normotensive and hypertensive subjects. Moreover, even among the hypertensive range of blood pressure, the higher the blood pressure is, the lower the sensitivity to pain is. These findings strengthen the hypothesis of a role of the degree of blood pressure elevation in modulating pain sensitivity.

Effects of sustained-release isradipine on left ventricular anatomy and function in systemic hypertension.

With use of digitized M-mode echocardiograms and 24-hour noninvasive ambulatory blood pressure (BP) monitoring, the effects of chronic treatment with sustained-release isradipine on left ventricular (LV) morphology and function in hypertensive patients were evaluated. We selected 12 patients with LV hypertrophy and normal LV diastolic diameter. Echocardiograms and 24-hour BP monitoring were performed after 2 weeks of placebo and after 6 months of oral treatment with sustained-release isradipine (5 mg once daily). Therapy significantly reduced BP without changes in heart rate. LV mass decreased in all patients and peak lengthening rate of LV diameter, index of diastolic function, increased in all, with normalization in 7 of the 9 with basal diastolic impairment. Peak shortening rate of LV diameter, index of systolic function, was normal in all patients at basal evaluation and did not change after therapy. Reduction in LV mass significantly (p < 0.05) correlated with the decrease in average 24-hour and daytime systolic and diastolic BP. Sustained-release isradipine administered once daily is an effective antihypertensive agent; the drug also induces regression of LV hypertrophy, with significant improvement in LV diastolic function and no deterioration in systolic function.

Effect of enalapril on left ventricular mass and performance in essential hypertension.

The effect of enalapril on left ventricular (LV) morphology and function was studied in 12 hypertensive patients. The subjects were evaluated after 2 weeks of placebo and after 4 months of treatment with enalapril (20 or 40 mg once daily), using M-mode digitized echocardiograms. The drug reduced arterial blood pressure in all patients. Systemic vascular resistance decreased significantly without changes in cardiac output and heart rate. No patient had significant side effects. After treatment LV mass decreased significantly (233 +/- 46 to 204 +/- 37 g, p less than 0.01); the reduction was due to a decrease in septal and posterior wall thickness, without changes in LV diameter. LV systolic function remained unchanged, whereas peak lengthening rate of LV dimension, an index of LV diastolic function, increased significantly (4.05 +/- 1.8 to 5.11 +/- 1.8 s-1, p less than 0.01). After treatment the basal inverse correlation between peak shortening rate and wall stress did not change, the inverse correlation between peak lengthening rate and wall stress became closer and the basal inverse correlation between peak lengthening rate and LV mass disappeared. In conclusion, antihypertensive treatment with enalapril led to a significant regression of LV hypertrophy associated with improvement in LV diastolic performance and no deterioration of LV systolic function.

Left ventricular function after reversal of myocardial hypertrophy in systemic hypertension, and response to acute increase of afterload by cold pressor test.

Using digitized M-mode echocardiography, the left ventricular (LV) response to acute increase in blood pressure after regression of myocardial hypertrophy due to an effective antihypertensive treatment was evaluated. Fifteen hypertensive patients with basal LV hypertrophy (LV mass greater than 230 g, and normal LV diastolic diameter) and normal LV mass after 3 to 4 months of treatment with angiotensin-converting enzyme inhibitors were selected for study. Subjects performed a cold pressor test before and after therapy. LV systolic function was normal in all subjects. LV diastolic function (impaired at basal evaluation in 13 subjects) improved after therapy in all subjects, with normalization in 10. Before treatment, the cold pressor test induced significant increases in blood pressure and heart rate without changes in LV parameters. After regression of hypertrophy, the cold pressor test induced increases in hemodynamic parameters comparable to those of the basal test, and LV parameters remained unchanged. Our results indicate that regression of myocardial hypertrophy induced by angiotensin-converting enzyme inhibitors does not impair the ability of the left ventricle to face acute increases in afterload. The improvement in LV diastolic function (found at rest after reversal of hypertrophy) persists during the cold pressor test, which confirms that it is primarily due to LV mass reduction and is not simply a consequence of decrease in afterload induced by treatment.

Left ventricular anatomy and function in normotensive young adults with hypertensive parents. Study at rest and during handgrip.

Using digitized M-mode echocardiograms, we evaluated left ventricular (LV) anatomy and function at rest and during handgrip in 24 normotensive young adults with both parents hypertensive (HP+), each matched for age, sex, body weight, and body surface area with one normotensive adult with both parents normotensive (HP-). LV parameters were within the normal range in all HP+ and HP-. At rest, HP+ as compared to HP- had higher systolic and diastolic blood pressure (BP), septal and posterior wall thickness, and LV mass; LV diastolic diameter and end-systolic wall stress were similar in the two groups. Modified midwall fractional shortening, peak shortening rate of LV diameter and peak thickening rate of LV posterior wall, indices of LV systolic function, and peak lengthening rate of LV diameter and peak thinning rate of LV posterior wall, indices of ventricular relaxation, were significantly higher in HP+. Handgrip induced significant (P < .001) and percent-comparable increases of systolic and diastolic BP, heart rate, and cardiac output in HP+ and HP-; peak shortening and lengthening rates of LV diameter and peak thickening and thinning rates of LV posterior wall increased significantly in HP-, whereas in HP+ the value of the four parameters, higher at rest as compared to HP-, did not show any further increase. In conclusion, normotensive young adults with high genetic risk for hypertension have higher BP and thicker and overactive LV as compared to subjects with normotensive parents. Handgrip stimulates LV function in offspring of normotensives, but not the already hyperkinetic LV of hypertensive offspring.

Determinants of left ventricular function before and after regression of myocardial hypertrophy in hypertension.

Using digitized M-mode echocardiograms, we evaluated the determinants of left ventricular (LV) systolic and diastolic function in 30 hypertensives with LV hypertrophy (LV mass > 230 g and normal LV diastolic diameter), before (LV mass 319 +/- 26 g) and after normalization of LV mass (196 +/- 21 g) by antihypertensive treatment with angiotensin converting enzyme inhibitors. As a control group we selected 50 normal subjects. Using multiple regression analysis we studied the relative role of preload (LV end-diastolic diameter), afterload (end-systolic wall stress), inotropic state (systolic pressure/end-systolic LV diameter ratio), and LV mass on LV systolic (peak shortening rate of LV diameter) and diastolic function (peak lengthening rate of LV diameter). The major determinant of systolic function was the end-systolic stress in hypertensives before treatment and the systolic pressure/end-systolic LV diameter ratio in normals and in hypertensives after treatment. The major determinant of diastolic function was LV mass in hypertensives before treatment and end-systolic stress in normals and in hypertensives after normalization of LV mass by treatment. Preload seems not to influence LV function in normals and in hypertensives with normal LV diameter. The inotropic state is the major determinant of systolic function in normals and in hypertensives after treatment, whereas this role is played by afterload in hypertensives before treatment. The diastolic function is primarily influenced by after-load in normals and in hypertensives after regression of myocardial hypertrophy, whereas in hypertensives with myocardial hypertrophy LV mass is the major determinant of diastolic function.

Microalbuminuria as a marker of preclinical diastolic dysfunction in never-treated essential hypertensives.

Using 24-h ambulatory blood pressure (BP) monitoring and digitized M-mode echocardiography, we evaluated whether microalbuminuria is related to preclinical left ventricular (LV) diastolic dysfunction in hypertensive patients. We selected 87 never-treated hypertensive patients (mean 24-h BP > 140 and/or > 90 mm Hg); albuminuria was evaluated as mean value of 24-h urinary albumin excretion (UAE) from two 24-h urine collections. Microalbuminuria was found in 28 patients, classified as MA+ (UAE 30 to 300 mg/24 h); 59 patients had normal UAE (< 30 mg/24 h) and were classified as MA-. The MA+ and MA- groups did not differ with regard to age, sex, body mass index, or 24-h heart rate, whereas 24-h, daytime, and nighttime systolic and diastolic BP were significantly higher in MA+ than in MA-. The LV mass index was greater in MA+, as was the prevalence of LV hypertrophy; peak shortening rate of LV diameter, index of systolic function, was normal in all, but was lower in MA+. Peak lengthening rate of LV diameter and peak thinning rate of posterior wall, indices of diastolic function, were lower in MA+ and the prevalence of diastolic dysfunction was higher in MA+. UAE was inversely correlated with both indices of LV diastolic function, also after correction for age, 24-h heart rate, 24-h BP, and LV mass. In conclusion, in never-treated hypertensive patients, microalbuminuria is not only associated with greater myocardial mass, but is also related with preclinical impairment of LV diastolic function. This relation, independent from increased BP or LV mass, strengthens the role of microalbuminuria as an early and reliable marker of preclinical cardiac involvement.

Double-blind comparison of perindopril and captopril in hypertension. Effects on left ventricular morphology and function.

Using digitized M-mode echocardiograms, we compared, in a double-blind study, the effects of 4 to 8 mg perindopril given once daily and 25 to 50 mg captopril given twice daily on the left ventricle (LV) in 20 hypertensive patients. Both treatments significantly (P less than .001) lowered blood pressure, reducing systemic vascular resistances. After 3 months both drugs induced a comparable percentage of reduction in LV mass, with an increase in the peak rate of LV relaxation and no changes in the peak rate of LV contraction. Our results demonstrate that perindopril once daily is an effective antihypertensive agent; it is also able, like captopril, to induce regression of LV hypertrophy, with improvement in diastolic performance and no deterioration in ventricular systolic function.

Hyperinsulinemia, family history of hypertension, and essential hypertension.

The aim of this study was the evaluation of the relationships among hyperinsulinemia, a family history of hypertension, and essential hypertension. Insulin and C-peptide responses to an oral glucose load were studied in 175 lean normotensives (N) and untreated hypertensives (H) with (F+) and without (F-) a family history of hypertension: 30 NF-, 30 NF+, 45 HF-, and 70 HF+. The groups were comparable for age, sex, body mass index, and blood pressure. The following parameters were evaluated: plasma glucose (G), serum insulin (I), and C-peptide (Cp) before and 30, 60, 90, and 120 min after the glucose load, fasting glucose/insulin ratio (ISI), fasting insulin/C-peptide ratio (I/Cp), and 24-h ambulatory blood pressure monitoring. Plasma glucose was measured, fasting and during the test, and it and I/Cp were similar in the four groups. Serum insulin and Cp, both fasting and stimulated, were significantly higher and ISI lower in normotensives and hypertensives with hypertensive parents. Grouping the subjects first on the basis of blood pressure and then on the basis of family history, no differences were found between normotensives and hypertensives, whereas I and Cp, fasting and stimulated, were significantly higher and ISI lower in subjects with positive as compared to negative family history. The closest correlations between insulin and ambulatory blood pressure were found in normotensive with hypertensive parents; in hypertensives with hypertensive parents we only found a direct correlation between fasting Cp and nocturnal blood pressure fall; in hypertensives with normotensive parents insulin inversely correlated with nocturnal blood pressure fall. Insulin resistance seems to have a familial basis, independently of the presence of hypertension. Instead of showing a causal relationship between insulin resistance and hypertension, our results indicate that the two are partly independent components of a common familial pattern.

Relationship between left ventricular diastolic function and atrial natriuretic factor in never-treated mild hypertensives.

Using digitized M-mode echocardiograms, we evaluated the relationship between plasma atrial natriuretic factor (ANF) and morphofunctional characteristics of the left ventricle (LV) in 24 mild hypertensive men, never treated, with normal renal function. For each subject we collected a blood sample for plasma ANF evaluation and, immediately after, we recorded the LV echocardiogram. All the patients had normal LV diastolic diameter and systolic function; LV hypertrophy was present in 10 patients, 7 of whom had left atrial enlargement, and 13 patients had impaired LV diastolic function. ANF was similar between patients with and without LV hypertrophy, as well as between patients with and without left atrial enlargement, whereas ANF was significantly (P < .01) higher in patients with LV diastolic dysfunction than in patients with normal diastolic function. ANF was inversely correlated with both indices of diastolic function (peak lengthening rate and peak wall thinning rate), whereas it did not correlate with blood pressure, heart rate, end-systolic wall stress, and other LV parameters. In conclusion, from our results, ANF level in never-treated mild hypertensives is related neither to the degree of LV hypertrophy nor to the afterload, expressed as blood pressure or end-systolic wall stress, whereas it is mainly influenced by LV diastolic function: the diastolic impairment induces an increase in ANF level, probably through an increased atrial stretch.

Microalbuminuria in never-treated hypertensives: lack of relationship to hyperinsulinemia and genetic predisposition to hypertension.

We evaluated the relationship of microalbuminuria to hyperinsulinemia and family history of hypertension in 92 never-treated essential hypertensives (mean 24-h blood pressure >140 or 90 mm Hg), with positive (F+) or negative (F-) family history of hypertension: 31 had microalbuminuria (MA+) (urinary albumin excretion [UAE], 30 to 300 mg/24 h) and 61 had normal (<30 mg/24 h) UAE (MA-). Glucose and insulin values before and 30, 60, 90, and 120 min after an oral glucose load were measured together with an index of peripheral insulin activity (10(4)/ insulin x glucose values at glucose peak). Subjects with and without microalbuminuria did not differ with regard to age, sex, body mass index, and 24-h heart rate, whereas 24-h, daytime, and nighttime systolic and diastolic blood pressure were significantly higher in MA+ than MA- patients. The prevalence of positive family history of hypertension was similar between MA+ and MA-, as were fasting and stimulated glucose and insulin values and the index of peripheral insulin activity. Subdividing the patients on the basis of family history of hypertension (59 F+, 33 F-) UAE was not significantly different between F+ and F-. UAE did not correlate with glucose and insulin parameters. From our results, in never-treated hypertensives, microalbuminuria is associated with higher blood pressure values, but is related neither to genetic predisposition to hypertension, nor to hyperinsulinemia; therefore, impaired insulin sensitivity and microalbuminuria are two components of the hypertensive syndrome, largely independent of each other.

Improved left ventricular function after short-term treatment with fructose-1,6-diphosphate: echocardiographic study in chronic ischemic heart disease and idiopathic dilated cardiomyopathy.

The effect of fructose-1,6-diphosphate (FDP) on left ventricular function was assessed in seven patients with chronic ischemic heart disease and eight patients with idiopathic dilated cardiomyopathy. In a crossover study design each patient received 10 gm of FDP or saline placebo intravenously for three days. An M-mode echocardiographic assessment of left ventricular (LV) function was made before and after each treatment period. After FDP treatment, LV end-diastolic and systolic dimensions showed a 6% reduction (P less than 0.01), while peak lengthening rate of LV dimension in diastole and peak shortening rate of LV dimension in systole increased 17% and 10%, respectively (P less than 0.05). There was evidence that FDP was more effective in the patients with ischemic heart disease than in the patients with cardiomyopathy.