Pier Luigi Malini

The use of a telematic connection for the follow-up of hypertensive patients improves the cardiovascular prognosis

Background Inadequate blood pressure (BP) control could be due to incorrect management of hypertensives caused by the lack of interaction between general practitioners (GP) and hypertension specialists. Objectives To test the effectiveness on BP and total cardiovascular risk (TCVR) control of an internet-based digital network connecting specialists and GPs. Methods We created a network among the Hypertension Clinic, Federico II University (Naples, Italy), 23 hospital-based hypertension clinics and 60 GPs from the area (CampaniaSalute Network, CS). Randomized GPs enrolled in CS could update online records of patients (n = 1979). As a control, we included 2045 patients referred to the specialist clinics by GPs from outside the network. All patients completed a 2-year follow-up. Results CS provided a larger reduction in BP [systolic/diastolic BP (SBP/DBP): 7.3 ± 0.4/5.4 ± 0.3 versus 4.1 ± 0.4/3.1 ± 0.26 mmHg, CS versus control; P < 0.001 for both] and percentage of patients with BP < 140/90 mmHg (CS versus control: baseline, 33 versus 34%, NS; end of follow-up, 51 versus 47%, χ2 = 13.371; P < 0.001). A European Society of Hypertension–European Society of Cardiology (ESH/ESC) TCVR score was calculated [from 1 (average) to 5 (very high TCVR)]. The CS group showed a reduction in the mean TCVR score (CS: from 3.5 ± 0.02 to 3.2 ± 0, P < 0.01, ANOVA; control group: 3.5 ± 0.03 to 3.4 ± 0.03, NS) and, accordingly, fatal and non-fatal major cardiovascular events (MACE) were less frequent (2.9 versus 4.3%; χ2 = 5.047, P < 0.02). CS predicts fewer MACE in multiple binary regression analysis (β:−7.27, P < 0.008) reducing the risk for MACE compared to control [odds ratio (OR): 0.838; 95% confidence interval (CI): 0.73–0.96]. Conclusion Our results support the idea that telemedicine can achieve better control of BP and TCVR.

Thromboxane antagonism and cough induced by angiotensin- converting-enzyme inhibitor

BACKGROUND The increased prostaglandin synthesis that might follow stimulation of the arachidonic acid cascade by angiotensin-converting-enzyme inhibition (ACE-I) has been suggested to underlie the appearance of cough on ACE-I treatment. We investigated whether the prostanoid thromboxane was involved. METHODS Nine patients with essential hypertension who had cough after enalapril 20 mg once a day (coughers) were treated, while continuing the enalapril, in a double-blind crossover study with placebo or picotamide, 600 mg twice daily. Picotamide is a platelet antiaggregant that acts through both inhibition of thromboxane synthase and thromboxane-receptor antagonism. Thirteen hypertensive patients with no history of ACE-I-induced cough were also treated with enalapril and served as controls. Cough frequency was measured by a visual analogue scale and by a daily cough diary. 24 h urinary recovery of 11-dehydro-thromboxane-B2 and 6-keto-PGF1 alpha were measured to assess any changes in endoperoxide metabolism during the study periods. FINDINGS 11-dehydro-thromboxane-B2 (TXB2) recovery was significantly reduced by picotamide, which led to the disappearance of cough in eight patients within 72 h. Picotamide urinary recovery data suggested incomplete absorption in the non-responder. At baseline and after rechallenge with enalapril, 11-dehydro-TXB2 excretion was in the same range in the controls and in the coughers, but the latter showed significantly lower excretion of 6-keto-PGF1 alpha, and their ratio of 11-dehydroTXB2 to 6-keto-PGF1 alpha was twice that of the controls (1.40 [95% CI 0.86-1.95] vs 0.61 [0.37-0.84]). INTERPRETATION A thromboxane antagonist is effective in ACE-I-induced cough. An imbalance between thromboxane and prostacyclin may represent a marker of patients susceptible to ACE-I-induced cough.

Cough during Treatment with Angiotensin Converting Enzyme Inhibitors

SummaryThe role of age, gender, smoking habits and concomitant drug treatment, and type and dose of angiotensin converting enzyme (ACE) inhibitor as prognostic factors for the development of cough during ACE inhibition was investigated in a group of 1591 patients. In 117 of these patients cough was identified as drug related. Logistic regression confirmed that females, nonsmokers and patients treated with enalapril are at greater risk of developing cough. On the other hand, our data provided no evidence for a prognostic role of higher doses of the ACE inhibitor or of concomitant drug treatment; in particular, the use of β-adrenoceptor antagonists was not associated with a higher incidence of cough.

Digitalis 'receptors' during chronic digoxin treatment.

1. The effect of digoxin treatment on Mg‐dependent [Na+‐K+]‐ATPase (the receptor for cardiac glycosides) was assessed by comparison of intracellular Na+‐K+, 86Rb uptake and number of digoxin binding sites in the erythrocytes of 138 patients on long term digoxin and of 133 control subjects. The parameters were also assessed in thirty‐two patients followed longitudinally for 1 y.

ACE Inhibition and Pressor Responsiveness to Norepinephrine in Hypertensive Patients

The pressor response to norepinephrine (NE) was assessed in normal renin essential hypertensive patients before and after they were randomly assigned to receive in parallel groups of treatment a single dose of an angiotensin converting enzyme (ACE) inhibitor (captopril or lisinopril) or a prolonged therapy with lisinopril (30–45 days) or with hydrochlorothiazide (9 days). Blood pressure was significantly reduced by all treatments. The pressor response to NE was unchanged after the single administration of the ACE inhibitors, while it was blunted after chronic administration of lisinopril and after the diuretic. On the basis of these results, it is suggested that the attenuation of the sympathetically mediated vasoconstriction may represent an additional mechanism contributing to the antihypertensive effect of ACE inhibitors administered chronically.

Indapamide or hydrochlorothiazide in hypertensive patients resistant to treatment with an angiotensin-converting enzyme inhibitor

Abstract This randomized, double-blind, parallel-group study evaluated combination therapy in 31 patients with mild-to-moderate hypertension whose blood pressure levels were not controlled by enalapril, 20 mg/d, monotherapy. Patients were divided into two groups. Group 1 (n = 15) continued enalapril and received indapamide, 2.5 mg/d; group 2 (n = 16) continued enalapril and received hydrochlorothiazide 25 mg/d. After 12 weeks of treatment, both combinations were equally effective in lowering blood pressure; normalized blood pressure levels were seen in 11 patients in each group. Decreases in serum potassium levels and increases in uric acid levels were significant in both groups. Triglyceride blood levels increased significantly more in the hydrochlorothiazide group than in the indapamide group; other metabolic parameters were unaffected by both treatments.

DIGITALIS RECEPTORS AND DIGOXIN SENSITIVITY IN RENAL FAILURE

1. The number and the in vitro and in vivo affinity of digitalis receptors for digoxin were measured in patients with normal renal function and in uraemics.

The effect of ace inhibition on peripheral hemodynamics in normotensive and hypertensive patients with type II diabetes.

The effect of treatment with enalapril (10 days at 10 mg/d followed by 4 weeks at 20 mg/d) on forearm hemodynamics was assessed in eight normotensive patients and eight patients with hypertension affected by Type II diabetes as well as in eight patients with essential hypertension and normal glucose tolerance. The ACE inhibitor decreased regional vascular resistances and increased the maximum arteriolar‐vasodilating capacity and venous distensibility in the three groups of patients. Thus, this study shows that ACE inhibition by enalapril improves regional hemodynamics in patients with Type II diabetes.