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Objective. To assess the effectiveness of rehabilitation in a group of patients with active ankylosing spondylitis (AS) by the Assessment in Ankylosing Spondylitis (ASAS) Working Group response criteria. [ABSTRACT FROM PUBLISHER]

Background Although individuals with diabetes mellitus frequently have dyslipidaemias and high blood pressure, much of the increased risk for coronary heart disease is not explained by these and other classical risk factors. Thus, other less widely recognized risk factors, including increased susceptibility of low-density lipoprotein (LDL) to oxidation, might enhance vascular dysfunction and atherogenesis in diabetes.Aims We compared both the rate and extent of LDL oxidation ex vivo between 78 poorly controlled individuals with type 1 diabetes and 78 age- and sex-matched non-diabetic controls. We then initiated intensive insulin therapy for 3 months to determine the impact of improved glucose control on LDL composition and oxidation.Results Diabetic and non-diabetic individuals did not have significantly different body weights, dietary intake, blood pressure, renal function or plasma lipid levels. LDL composition was also similar in both groups. In contrast, vitamin E content in LDL was significantly lower in diabetic patients. Measures of LDL lipid oxidation, including conjugated diene, lipid peroxide and thiobarbituric acid reactive substances formation, as well as measures of LDL protein modification, were significantly greater in diabetic patients. Levels of hyperglycaemia correlated strongly with each measure of LDL lipid oxidation (r ranges from 0·60–0·81,P <0·05 for each correlation). After improved glucose control (average reduction in % HbAlcof 5·5 units) all measures of LDL oxidation improved dramatically and approached values for non-diabetics. Absolute values of LDL oxidation increased among all categories of age in both diabetic and control individuals, and this relationship persisted even after adjustment for differences in glucose concentrations.Conclusions We demonstrate that hyperglycaemia has a potent but reversible effect on LDL oxidation and that age may independently enhance LDL susceptibility to oxidation. These pathophysiological effects may play an important role in determining vascular complications and atherogenesis in poorly controlled type 1 diabetic patients. [ABSTRACT FROM PUBLISHER]

Acidosis is associated with myocardial ischemia and several reports indicate the greater vulnerability of the aged heart to ischemic dysfunction. We investigated the effects of hypercapnic acidosis on isolated heart (n = 14) and papillary muscle (n = 10) from adult and senescent rats. Acidosis (pH from 7.36 to 6.91) induced a decrease in left ventricular developed pressure together with an increase in left ventricular end-diastolic pressure, but was significantly more evident in senescent than in adult hearts (p < .01). The return to normal pH induced a further increase in the end-diastolic pressure parallel to the development of arrhythmias that were greater in senescent than in adult hearts. In isolated papillary muscle, acidosis confirmed its greater negative inotropic effect on senescent than adult muscles (p < .01), while intracellular sodium activity (aNai) increased to a similar extent in both adult and senescent papillary muscles (p = NS). 5-(N,N-dimethyl)-amiloride hydrochloride (DMA), a specific inhibitor of Na+/H+ exchanger, produced similar modification of tension and aNai in both adult and senescent muscles. When DMA was superfused in acidotic solution, the contractility was markedly compromised in senescent than in adult muscles (p < .01), but the aNai modifications were similar in adult and senescent muscles (p = NS). Our results show that acidosis induced a greater reduction of contractility in senescent than in adult hearts. The similarity of contractility during DMA administration between adult and senescent muscle and of modifications of aNai suggests that depression of contractility with acidosis may be related to pathophysiologic mechanisms other than the Na+/H+ exchanger. [ABSTRACT FROM AUTHOR]

Background: Sarcolemmal Na(+)-Ca2+ exchange system is believed to be fundamental to the control of cardiac contractility. However, the relation between Na(+)-Ca2+ exchange and the control of contractile force has not been studied in senescent myocardium.Methods: The role of Na(+)-Ca2+ exchange in the regulation of the cardiac muscle's contractile force was studied in adult and senescent papillary muscles by simultaneously measuring intracellular sodium activity (aNai), action potential, and contractile force while varying extracellular concentration of sodium and/or calcium.Results: Reduction of [Na+]o decreased aNai from 8.0 +/- 1.8 to 4.1 +/- 0.8 in adult (-3.9 mM) and from 8.7 +/- 1.9 to 4.7 +/- 0.9 in senescent (-4.0 mM) papillary muscles, while developed tension (DT) increased by 80.2% in adult and by 135.6% in senescent papillary muscles (p < .01 vs adult). During low [Ca2+]o and high [Na+]o, aNai and DT modifications were similar both in adult and senescent papillary muscles. During high [Ca2+]o, aNai decreased to a similar extent in both adult and senescent papillary muscles, while DT increased by 37.8% in adult and by 67.8% in senescent (p < .05 vs adult). Simultaneous reduction of [Na+]o and [Ca2+]o decreased aNai from 8.1 +/- 1.2 to 6.8 +/- 1.1 mM in adult (-1.3 mM), and from 8.4 +/- 1.0 to 7.2 +/- 1.0 mM in senescent (-1.2 mM) papillary muscles while DT decreased by 22.1% in adult and by only 12.0% in senescent (p < .01 vs adult) papillary muscles. Simultaneous increase of [Na+]o and [Ca2+]o similarly increased aNai in both adult senescent papillary muscles, but decreased DT by 28.5% in adult and by 11.7% in senescent (p < .01 vs adult). After [Na+]o modifications, the equilibration time for the ratio of external and internal sodium ion activities was slowed in senescent papillary muscles (i.e., in low [Na+]o solution the equilibration time was 4.6 +/- 0.9 min in adult and 6.3 +/- 1.2 min in senescent papillary muscles, p < .001).Conclusions: Similar changes of aNai during transmembrane Na+ and Ca2+ gradients modifications associated to changes in contractile force seem to demonstrate that Na(+)-Ca2+ exchange is probably not modified by the aging process. However, the slow equilibration time for the ratio of Na+ activities might reflect an age-related reduction of the Na(+)-K+ pump activity. [ABSTRACT FROM AUTHOR]

Background: We studied the effects of age and hypertension on responses to chronotropic dose (CD25) and standing-induced changes in the ratio of electrical systole (QT) to electromechanical systole (QS2) in order to identify their role on beta adrenoceptor sensitivity and to verify the value of QT/QS2 ratio as a noninvasive parameter of beta-adrenoceptor sensitivity.Methods: We enrolled 33 normal subjects and 37 hypertensive patients (WHO stage I and II) (age range 21-82 years).Results: CD25 was significantly age-related in normotensive and hypertensive subjects, whereas standing-induced QT/QS2 changes were age-related in normotensive subjects only When we divided subjects into three age groups, beta-adrenoceptor sensitivity was found to be lower in hypertensives than normotensives in the two groups under age 60, but was not affected in those over age 60. This suggests that hypertension influences beta-adrenoceptor sensitivity in younger subjects, but not in elderly patients, whose beta-adrenoceptor sensitivity is already reduced.Conclusions: CD25 does not predict standing-induced QT/QS2 ratio changes; therefore, during autonomic stimulation, QT/QS2 ratio seems not to be significantly related to beta adrenergic sensitivity. [ABSTRACT FROM AUTHOR]

This study was designed to investigate the effect of heart rate changes on dipyridamole echocardiographic tests in patients with coronary artery disease treated with propranolol. We prospectively studied 12 patients (8 men and 4 women; mean age 56.5 ± 8.7 years) selected by: (a) angiographic evidence of significant coronary artery disease; (b) adequate echocardiographic window; (c) positive dipyridamole echocardiography test results in baseline conditions (step I); (d) test reproducibility in the absence of treatment; (e) negative dipyridamole echocardiography test results after 7 days of treatment with propranolol (120 mg. day) in twice divided doses daily (step II). In all patients treated with propranolol, dipyridamole echocardiographic testing was repeated 24 h after the last negative test. In these patients, transoesophageal atrial pacing was performed at peak dipyridamole infusion to increase heart rate to values similar to those observed at baseline (step III). At baseline, heart rate and rate-pressure product were significantly lower in patients treated with propranolol (− θ20.3% and − θ22.5% in group II, P<0–001 vs step I; − θ24.3% and − θ26.4% in group III, P<0.05 vs step I), but the different treatments did not produce significant differences in systolic and diastolic blood pressure. At peak dipyridamole infusion, heart rate and rate-pressure product increased with either placebo or propranolol treatments with respect to baseline, while remaining significantly lower with propranolol as compared to placebo ( − θ29.6% and − θ29.5% in step II, P<0001). During treatment with propranolol plus transoesophageal pacing to maintain heart rate at values attained with placebo, the rate-pressure product did not change significantly with respect to placebo, nor did systolic blood pressure. Transoesophageal atrial pacing performed during propranolol treatment to restore heart rate to baseline values did not affect the dipyridamole echocardiographic test in eight patients (group I), and induced transient wall abnormalities in four patients (group II) (P= θns). Our data suggest that the anti-ischaemic effect of propranolol in man is not correlated only to reduction of heart rate. [ABSTRACT FROM PUBLISHER]

We evaluated the acute therapeutic effects of the oral administration of n (10mg) and diltiazem (120 mg) alone and in combination in 16 patients with effort angina. The 16 patients (13 men and three women; mean age 59±7 years) performed a symptom-limited bicycle exercise stress test 3 h after placebo or active substance administration. Maximal work load, exercise duration and time to 1 mm ST segment depression were significantly increased and ST depression at peak exercise was significantly decreased by the combination of drugs. N and diltiazem alone similarly improved exercise duration as markedly as their combination. One patient stopped the test after all three treatments for angina associated with ST depression > 2mm. The combination of drugs yielded the best symptomatic effect: only four patients complained of angina in comparison to eight and seven patients after diltiazem and n respectively. Nifedipine and diltiazem are effective and safe antianginal drugs. Some patients respond better to one drug than to the other. Patients who remain symptomatic in spite of maximal doses of a single drug may derive some benefit from combination therapy. [ABSTRACT FROM PUBLISHER]

This study was performed to determine if QT prolongation before and during early exercise is related to the occurrence of exercise-induced ventricular arrhythmias (EIVA). EIVA occurred in 47 of 142 patients with angiographic evidence of coronary artery disease (CAD); no EIVA occurred among the 22 patients without CAD (OV). Resting QTc and QT intervals during early exercise were similar in patients without EIVA, irrespective of the presence or absence of CAD; however resting QTc was significantly longer in CAD patients who showed EIVA (443±40ms; ?<0·01) than in CAD patients without EIVA (424 ± 37 ms) and in OV patients (421 ±32 ms). During early exercise, the QT interval remained significantly longer in patients with than in those without EIVA. There was a trend toward increasing resting Q Tc in patients who exhibited EIVA more severe than grade 3. When resting QTc was longer than 440 ms, subsequent EIVA were correctly predicted in CAD patients with a sensitivity of 43%, a specificity of 72% and a predictive accuracy of 63%. Thus, a trend toward longer resting QTc values exists in CAD patients who develop EIVA; however, a long resting QTc (> 440 ms) appears to be only a weak predictor of subsequent EIVA. [ABSTRACT FROM PUBLISHER]

Objective: The contractile response to digitalis and β adrenoceptor agonists is lower in the senescent than in the adult myocardium, while the development of ventricular arrhythmias is increased. The aim of this study was to examine the effects of aging on cardiac response to digitalis and an adrenergic agonist used clinically. Methods: The electrical and mechanical responses were tested in isolated and perfused hearts from 3-24 month old rats receiving 15 min infusion of digitalis drug (ouabain, 6 × 10−5 M) alone, and after 5 min of β adrenoceptor agonist drug (epinine, 1.5 × 10−7 M). Results: Ouabain action was associated with a rise in left ventricular end diastolic pressure (p<0.01) which increased progressively with aging, and with an elevation of left ventricular developed pressure (p<0.01) which decreased progressively with aging. Epinine induced a reduction of left ventricular end diastolic pressure (p<0.01) and a rise in left ventricular developed pressure (p<0.01) but both effects decreased progressively with aging. Ouabain reduced coronary flow and this decrease was more pronounced with aging (p<0.01), while epinine caused an increase (p<0.01) that diminished in older hearts. Ouabain given after epinine resulted in a greater increase in left ventricular end diastolic pressure than epinine (p<0.01) but lower than that caused by ouabain alone (p<0.01), a greater increase in left ventricular developed pressure than epinine and ouabain (p<0.01), and a smaller reduction of coronary flow rate than ouabain alone (p<0.01). All these effects, however, diminished progressively with aging. Arrhythmia scores were higher during ouabain than in control (p<0.01) and in epinine treated hearts (p<0.01); pretreatment with epinine did not modify arrhythmia score during ouabain administration. The number and severity of arrhythmias, however, increased with aging in all groups. Conclusions: Aging has a negative effect on both the positive inotropic and the arrhythmogenic effects of ouabain and epinine, although these phenomena are more pronounced during ouabain administration. However, when the two drugs are given simultaneously, epinine does not modify the arrhythmogenic effect of ouabain but reduces some of its deleterious haemodynamic effects.Cardiovascular Research 1994;28:358-364 [ABSTRACT FROM PUBLISHER]

It has been previously reported that an increase in diastolic blood pressure greater than 15 mmHg comparing values at rest with those on treadmill exercise, with or without ST changes, enhances the probability of coronary artery disease. To investigate whether the diastolic blood pressure variation keeps its diagnostic value during upright bicycle exercise, we evaluated the diastolic blood pressure variations in 111 patients with angiographically documented coronary artery disease without previous myocardial infarction and in 53 patients with normal coronary arteries undergoing maximal stress testing on a bicycle ergometer. The sensitivity of diastolic blood pressure (DBP) variations to detect coronary artery disease was 66%, the specificity 32%, the positive predictive value 67%, the negative predictive value 31% and the predictive accuracy 55%. The respective values for ST depression were 83% (<0·001 vs DBP variations), 53% (<0· vs DBP variations), 64% (<0·05 vs DBP variations) and 75% (<0·001 vs DBP variations). Forty-nine of the 75 patients with multivessel coronary artery disease and 60 of the 89 patients without coronary artery disease or with single vessel disease had abnormal DBP variations (sensitivity 65; spec 33%). The sensitivity of ST segment depression in predicting multivessel disease was 91% (<0·001 vs DBP variations), and the specficity 42%. Thus for bicycle ergometer exercise testing, ST segment depression seems to be more accurate than DBP variations in the diagnosis of coronary artery disease. [ABSTRACT FROM PUBLISHER]

Background: A reduction of exercise-induced ischemia in patients with coronary artery disease by means of brief period of exercise followed by resting is called the "warm-up" phenomenon. This phenomenon may represent a clinical counterpart of "ischemic preconditioning." We studied the warm-up phenomenon in both adult and elderly patients with similar angiographic evidence of coronary artery disease, using three exercise tests after excluding the "training effect."Methods: In order to verify the presence of "training effect," three exercise tests were performed in days 1, 2, and 3 ("training" tests). The third test was used as baseline for a successive test, performed after a recovery period of 10 minutes to reestablish baseline electrocardiographic conditions. A third exercise test was performed 30 minutes later ("warm-up" tests).Results: "Training" tests did not differ in all parameters in both adult and elderly patients. "Warm-up" tests showed that time to onset 1-mm ST depression was significantly higher (p < .001). whereas ST depression and time to recovery was significantly lower in the second and third test in adult but not in elderly patients (p < .001 ). Difference (in seconds) in the time at which 1-mm ST depression occurred on first warm-up exercise compared with the second was inversely correlated with age (p < .001 ).Conclusions: Previous exercise followed by resting is able to reduce the successive exercise-induced ischemia ("warm-up" phenomenon) in adult but not in elderly patients with coronary artery disease. This is independent of a greater age-related severity of coronary disease and of "training effect." These results confirm the hypothetical age-related reduction of "ischemic preconditioning" in aging heart. [ABSTRACT FROM AUTHOR]

The authors describe a case of spontaneous angina during catheterization in a patient with left anterior descending and circumflex stenosis promptly relieved by diltiazem, 10 mg, given in the left ventricle. Coronary and systemic haemodynamics measured during and at the end of angina demonstrated an increase in blood flow to the ischaemic myocardium as the mechanism responsible for the diltiazem-induced angina relief. [ABSTRACT FROM PUBLISHER]