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Objectives: The aim of this study was (1) to measure adherence in males and females with uncontrolled hypertension, and (2) to identify factors associated with non-adherence to antihypertensive medication., Patients and Methods: Each general practitioner (GP) should include the first two male and the first two female patients with uncontrolled treated hypertension. Adherence to antihypertensive treatment was estimated by the GP and using the French League Against High blood pressure (FLAH) self-administered questionnaire. A stepwise logistic regression analysis was used to identify factors associated with non-adherence on the FLAH scale, independently in males and in females., Results: A total of 1630 males and 1612 females were included in the analysis. Adherence to treatment was significantly better in females or when estimated by the GP. Lack of motivation was the first factor associated with poor adherence in both sexes. Considering hypertension as a simple anomaly and not a disease that can lead to cardiac or cerebral disorders was the second common parameter in both sexes. Other common factors were: having monthly periods of financial difficulties in facing his/her needs and absence of regular screening for colon cancer., Conclusion: Adherence to treatment is better in uncontrolled hypertensive females. Poor adherence is mainly associated with non-clinical factors. The lack of motivation is the most important element., (Copyright © 2015 Elsevier Masson SAS. All rights reserved.)

High blood pressure is a frequent pathology with many cardiovascular complications. As highlighted in guidelines, the therapeutic management of hypertension relies on non-pharmacological measures, which are diet and regular physical activity, but both patients and physicians are reluctant to physical activity prescription. To acquire the conviction that physical activity is beneficial, necessary and possible, we can take into account some fundamental and clinical studies, as well as the feedback of our clinical practice. Physical inactivity is a major risk factor for cardiovascular morbidity and mortality, and hypertension contributes to increase this risk. Conversely, regular practice of physical activity decreases very significantly the risk by up to 60%. The acute blood pressure changes during exercise and post-exercise hypotension differs according to the dynamic component (endurance or aerobic and/or strength exercises), but the repetition of the sessions leads to the chronic hypotensive benefit of physical activity. Moreover, physical activity prescription must take into account the assessment of global cardiovascular risk, the control of the hypertension, and the opportunities and desires of the patient in order to promote good adherence and beneficial lifestyle change., (Copyright © 2014 Elsevier Masson SAS. All rights reserved.)

The use of "snus" (smokeless tobacco) can be detrimental to health. Snus delivers rapidly high doses of nicotine which can lead to addiction. The use of snus increases the risk of myocardial infarction and stroke. Nicotine substitution therapy as well as bupropion and varenicline reduce withdrawal symptoms and tobacco craving during snus cessation. However, they have been shown not to assist in long-term abstinence. Information concerning potential cardiovascular hazards of snus must be incorporated into health educational programs in order to discourage its use. Snus is not a recommended product to help stop smoking., (Copyright © 2011 Elsevier Masson SAS. All rights reserved.)

The authors reviewed some of the most relevant studies dedicated to the assessment of the effects of the antihypertensive drugs on the stress-induced cardiovascular changes. The rises in both blood pressure and heart rate turned out not to be significantly altered by calcium channel blockers, ACE inhibitors, moxonidine, nor beta-blockers, whereas they seemed to be slightly blunted by alpha-blocking drugs. However, since baseline blood pressure was significantly lower in treated hypertensives than in placebo-given patients, all antihypertensive drugs eventually resulted in a lower blood pressure level during stress, as compared with untreated patients. Regarding white coat effect, which has to be considered as a very particular stress, it appeared to be lowered to the same extent by placebo and antihypertensive drugs; moreover, its changes were not associated with any clinical beneficial effect.

Harmonic imaging is an innovative technique which is now available in most of the echographic equipment currently on the market. The use of echographic contrast agents led to the introduction of this particular technology, which has largely superseded the former method. In everyday medical practice, it seems to provide a better definition of endocardial contours. In this article, the authors have described a prospective study including 32 patients with an average age of 64 years (+/- 5 years). The aim was to compare imaging quality obtained by 2 acquisition frequencies for standard imaging with that procured by harmonic imaging (emission and reception frequency, 2.5 and 3.3 MHz respectively for the former technique; emission and reception frequency, 1.7 and 2.2 MHz respectively for the latter). The overall scores given by 2 different examiners for emission and reception frequency were as follows: 3.28 and 3.15 for 2.5 MHz, 2.84 and 2.56 for 3.3 MHz regarding the standard technique; 2.56 and 3.031 for 1.7 MHz and 2.56 and 2.063 for 2.2 MHz for the harmonic imaging technique. The superior performance of tissue harmonic imaging has been confirmed in the endocardial study of the left ventricular segments and in the analysis of the mitral valve. This study shows that harmonic imaging, a technique which was easy to use in the present study, provides a means of obtaining an average level of ultrasound imaging that facilitates the interpretation of the clinical picture.

The cardiac cycle, as revisited by modern authors, consists of 3 fundamental phases: contraction, which includes isovolumic contraction and first part of ejection; relaxation which begins with left ventricular peak pressure, continues with second part of ejection and isovolumic relaxation, and ends together with ventricular rapid filling (i.e. as filling rate has decreased by 50 p. cent); finally compliance or slow filling which lasts until atrial systole. The LV diastolic dysfunction refers to filling abnormalities which are related to either relaxation abnormalities or compliance troubles or both. The mechanisms of these abnormalities are biochemical (deficiency in cyclic AMP resulting in calcium handling dysregulation) and mechanical: right ventricular filling, pericardial restraint, coronary arteries perfusion, myocardial inertial forces, myocardial visco-elastic properties, ventricular wall elasticity (depending itself on its thickness and its collagen content). The methods of analysis of LV filling are: left ventriculography, gamma angiography, digitized M-Mode echography and, mainly, Doppler echocardiography. This technique allows 2 types of mitral flow abnormalities to be distinguished: 1) the abnormal relaxation which combines an increased isovolumic relaxation time, an increased deceleration time and a diminished E/A ratio, but this pattern may be "normalized" by an increase in filling pressure; 2) the restriction to filling which results in an increased E/A ratio, a diminished deceleration time and, sometimes, a diastolic mitral regurgitation. The effects of drugs on LV diastolic function are difficult to assess: a beneficial result may be due either to a direct effect on the myocardium or to an improvement in load conditions, heart rate or contractility.

The authors have studied the effects of Nitrendipine, orally given in a dose of 20 mg, once a day for 30 days, in patients with mild to moderate hypertension. Twelve patients initially entered the study but four of them discontinued the treatment during the first week, because of unwanted side-effects: headaches, palpitation, sensations of burning skin. The remaining eight patients underwent a comparative evaluation at the end of a placebo period (DO) and at the end of the active treatment (D30), including successively: an automatic blood pressure recording with a Bard-Sentron device for 3 hours, then a determination of plasma renin activity, aldosterone and catecholamines, and finally a measurement of the blood pressure with a mercury manometer, at rest and during a standardized exercise on an ergometric bicycle. At D30, the Nitrendipine tablet was given one hour after the beginning of the automatic recording. The blood pressure measured with the mercury manometer (i.e. approximately 2 hours after the dose of Nitrendipine) significantly decreased from D0 to D30, at rest and during exercise, respectively from 161.5/104.6 to 132.8/82.5 mmHg and from 210.0/116.8 to 190.0/95.6 mmHg. The automatic recording provided, at D0, a mean blood pressure value of 152.4/90.6 mmHg; at D30, this mean value was as high as 142.6/90.7 mmHg during the hour preceding the dose of Nitrendipine (NS) and as high as 129.2/78.6 mmHg during the 2nd hour following the intake of the tablet (p less than 0.01). Plasma aldosterone and plasma renin activity significantly (p less than 0.05) increased from D0 to D30, whereas catecholamines did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Ambulatory measurement of the blood pressure may be considered as a reliable technique. Its validity is demonstrated by two types of factors: the first is physiological: the nycthemeral curves obtained with this method are similar to those provided by the first invasive studies, and especially show a definite nocturnal depression in most individuals; the second is epidemiological: the ambulatory blood pressure level is closely correlated with the left ventricular mass, measured on sonograms and has a good predictive value of future cardiovascular accidents. Its superiority over the standard measurement method, lies in the very principle of the method. It is an automatic measurement: the "white coat" artefact is therefore avoided. It is a repetitive and prolonged measurement, permitting therefore to analyze a complete nyctohemeral cycle instead of a single sample. Finally, it is an ambulatory measurement: the patients is therefore in his usual environment and not in the peculiar context of a medical office. However, the limitations of the method must be presented. The most important result from the interpretation of the collected data: the so-called aberrant values are identified from very arbitrary criteria and their elimination may be at the origin of errors; the currently available "norms" are only a indication and do not enable the physician to decide decisively between abstention and therapeutic intervention. An ambulatory blood pressure recording is particularly justified in the following two circumstances: 1) definite dissociation between elevated blood pressure at the consultation and moderate visceral repercussions; 2) hypertension resisting to an apparently well managed treatment that one hesitates to increase.

Sixteen patients with mild to moderate hypertension were randomized to receive either atenolol 100 mg a day (group A: 2 females, 6 males, mean age 42.3 years) or betaxolol 20 mg a day (group B: 8 males, mean age 49.3 years), both drugs given once daily for one month with a wash out on the 5th day. Pretreatment blood pressure was significantly higher in group B than in group A: this disparity, linked with randomization, hampered the comparison of the antihypertensive efficacy of both drugs but not the comparison of their pharmacodynamics. The maximal effect on resting supine blood pressure occurred later with betaxolol (4th day) than with atenolol (1st day), while the effect on peak exercise-blood pressure and heart rate was rapidly maximal (1st day) for both beta-blockers. The duration of the antihypertensive action at rest seemed to be nearly similar, while the effects of betaxolol on exercising heart rate and blood pressure were more prolonged than those of atenolol: on the wash out day, plasma atenolol and betaxolol levels fell in a same way but the increase in peak systolic blood pressure was more marked in group A than in group B, so that the positive correlation we found between the plasma drug levels and the percentage of peak systolic blood pressure reduction, was much closer with atenolol (p less than 0.001) than with betaxolol (p less than 0.05).

67 patients presented with a syncope of unknown origin following the usual exploration and were the subject of a more elaborated study: echocardiography (echo 2D) and Holter. 3.5 per cent of the Holter recordings enabled to ascribe to the heart the cause of the syncope. More than half of the Holters disclosed abnormalities of the cardiac rhythm leading to an anti-arrhythmic therapy in some cases, even when the cardiac origin of the loss of consciousness (LC) could not be confirmed. Echocardiograms could not lead to the diagnosis and less than one fourth of them disclosed abnormalities. In a developing study (14.8 +/- 8.7 months) that was carried out, 3 out of 4 patients did not present with any more LC; 3 died (6%) and 9 (18%) had LC again. On the other hand, in 5 patients (10%) a diagnosis could be evoked at the end of this follow-up. This study confirms the difficulties of diagnosis of this group of syncope of unknown etiology, as evidenced by the low results of intense and costly explorations and the little information obtained, even after a follow-up of more than 1 year.

112 echocardiographies and 91 long-term Holter recordings were performed looking for an emboligenic cardiac lesion in patients in sinus rhythm and free of any major carotid atherosclerosis. The results were evaluated in relation to the emboligenic potential of the lesions observed. 5 positive results were obtained (4.46%) on echocardiography (3 aneurysms of the interatrial septum, 1 myxoma and 1 endocarditis) and 10 positive results (10.99%) were demonstrated on the Holter monitor. Among the 45 (40.18%) echocardiographic anomalies capable of constituting a cardiac site of origin of emboli, there were 18 cases of dilatation or hypertrophy of the left chambers of the heart, 13 cases of calcification of the aortic valve, 8 cases of prolapse of the mitral valve and 8 cases of calcification of the mitral ring. Finally, 55.35 per cent of the echocardiographic examinations and 52.74 per cent of the Holter examinations were found to be normal. Although the yield of these examinations is low, the anomalies discovered were definitely responsible for the cerebral emboli and could only have been demonstrated by such investigations.

91 symptomatic patients were given an exercise test on a bicycle ergometer and a coronary arteriography test within a delay of 31 days. Of the patients (13 females and 78 males), 35 presented with a normal coronary arteriography and 56 presented with a pathological coronary arteriography (16 of whom had a history of myocardial infarction). We have studied the diagnostic value of several parameters taking into account changes in R waves upon exercise in V4 V5 V6 and changes in S waves in V1 V2. The most reliable parameter is also the easiest to calculate: it is considered positive when the R wave measured in V5 increases or does not change in the minute following cessation of exercise, as compared with the reference trace; it is considered negative when the R wave decreases. This criterion has a specificity of 60 per cent and a sensitivity of 71.4 per cent, and its diagnostic value is not improved by exclusion of patients with a history of infarction, or by exclusion of treated subjects or females. The horizontal or downsloping depression of the ST-segment has the same sensitivity but a better specificity (74%). Literature data are contradictory: some authors report that changes in the R wave upon exercise have a better predictive value than changes in the ST-segment, whereas an equal number of authors consider that the ST-segment is more informative. These differences of opinion result from methodological disparities and the large number of physiopathological elements affecting the amplitude of R waves.

Antihypertensive treatment may, for the same effect on hypertension, have a very different influence on the cerebral blood flow and the autoregulation curve. For instance, sodium nitroprusside, a potent vasodilator, risks to be poorly tolerated from the cerebral standpoint, when the sympathetic system is not inhibited. Diazoxide has no direct vasodilating effect on the cerebral vessels but, because of its marked hypotensive action must be used in divided doses. Hydralazine, a strong vasodilator, must be avoided in case of cerebral edema and hypertensive encephalopathy. Diuretics and beta-blockers, on a long-term basis, do not significantly modify the cerebral blood flow while alpha-methyl-dopa would increase it and facilitate a return to normal of the autoregulation curve. Captopril has demonstrated experimentally, interesting properties: in anaesthetized rats, it shifts the autoregulation curve to the left, i.e. toward lower pressures and it reduces the autoregulation curve to the left, i.e. toward lower pressures and it reduces the autoregulation limits; in awaken subjects, the decreased lower limit is also observed, explaining the good central tolerance of marked blood pressure reductions; on the contrary, its effects on the upper limit of the plateau are, unquestionably, counterbalanced by the effects of sympathetic stimulation concomitant with sudden blood pressure rises. As for calcium inhibitor, they do not seem to influence the long-term autoregulation of the cerebral flow.

Recent advances in medical technology have made it possible to non invasively record ambulatory blood pressure over 24 hours. This new method of measurement has a lot of advantages over the classic way: it enables a satisfactory approach of blood pressure circadian rhythm; it seems to be more reliable than clinic readings of blood pressure, which may be subjects to some confounding variables (e.g. observer bias, digit preference, defence reaction...); it appears to be better at predicting cardiovascular prognosis of hypertensive patients and is more closely correlated with target organ damage; finally, in some instances, it may help the physician to determine whether or not antihypertensive treatment should be initiated or adjusted. The limits and drawbacks of the method are also pointed out and, from a practical point of view, some recommendations are given to perform it only in most relevant circumstances.

The authors present 8 cases of aneurysms of the interauricular septum (AIAS). The diagnosis was established in all cases by two-dimensional echocardiography (E2D) which was requested, three times following a cerebral vascular accident (CVA). The AIAS manifest themselves as localised "hernias" of the inter-auricular septum, mobile during the cardiac cycle. Their topography was strictly right inter-auricular in 6 cases, whereas in the other 2 patients the AIAS passed into the left atrium at protosystole and returned to the right atrium at telesystole. Catheterization with angiography was carried out 5 times: the inter-auricular septum was crossed 4 times without gasometric reasons for an associated shunt; the AIAS was opacified in all cases. An anti-coagulant treatment was prescribed for 3 patients who had suffered a CVA, and for a fourth presenting numerous supraventricular extrasystoles which were sometimes grouped. A review of the literature of the last fifty years enabled a compilation of 93 cases of AIAS to be made, 49 of which had been examined by E2D, 35 had had a hemodynamic and angiographic exploration and 47 an anatomical and/or surgical confirmation. The main results obtained are described and commented on. The diagnostic, etiopathological and prognostic problems raised by the "updating" of this pathology are discussed.

The cerebral blood flow is maintained at a constant level in spite of blood pressure variations, because of a very performing auto-regulation phenomenon: vasoconstriction in case of elevated blood pressure, vasodilatation in case of blood pressure drop. The upper limit of the mean blood pressure beyond which nothing can prevent the cerebral blood flow from increasing, ranges between 150 and 170 mmHg. The lower limit, from which the dilatation of the cerebral blood vessels is not able to prevent the decreased cerebral blood flow, has been set between 50 and 70 mmHg. The auto-regulation of the cerebral blood flow is influenced by numerous factors: hypercapnia, hypoxia and ischemia complete inhibit it, making the cerebral blood flow directly related to the blood pressure; the sympathetic stimulation shifts the entire curve toward the right, because of the constriction of the pia-mater arteries, followed with a reactional vasodilatation of the small cerebral vessels. In the course of chronic arterial hypertension, the same shift of the auto-regulation curve toward high pressures is observed, related to structural alterations of the vascular wall; this make them more prone to constriction than dilatation: when these alterations are reversible, antihypertensive treatment may sometimes bring the auto-regulation curve in its initial position.

The authors have compared the anti-arrhythmic activity and tolerance of disopyramide and amiodarone in the treatment of ventricular extrasystoles (VES) by using two quantitative methods of assessment. The stability of the rhythmic disorder was confirmed by two control Holter recordings in 20 patients without treatment, 16 of whom were bearers of an organic cardiopathy. The ventricular extrasystole was greater than 90 VES/hour in 18 patients. After the first control, Holter recording, each patient was treated successively with 400 mg of disopyramide/day in 4 doses for average period of 31 days, then a second Holter control recording without treatment, then 600 mg/day of amiodarone for 8 days followed by a maintenance dose varying from 200 to 400 mg/day: this second period of treatment lasted for an average of 38 days. The reduction of the number of VES was greater than 65 percent (SAMI criterion) in 2 of the 20 patients treated with disopyramide and in 13 of the 20 patients treated with amiodarone. Using the method of variance analysis, disopyramide was found to be efficacious in 5 cases out of 20 and amiodarone in 15 cases out of 20. Both methods indicate that the greater efficacy of amiodarone is statistically significant (p less than 0.01). All of those who did not respond to amiodarone were also non-responders to disopyramide.

We studied the simultaneous effects of nifedipine on the pulmonary circulation and blood gases in 12 patients with pulmonary hypertension secondary to obstructive chronic bronchitis. Measurements were carried out at rest and during stress, initially then one hour after administration of 20 mg of nifedipine sublingually. They were repeated in a similar fashion after a 6-month treatment with 60 mg/day (group II) (30 mg/day in case of intolerance) (group I). The results of the immediate effect of nifedipine are in favor of a passive pulmonary vasodilatation secondary to the systemic vasodilatation. After six months of treatment, the pulmonary vasodilatation persists, but is associated with a decreased motor pressure indicating a more specific and more active pulmonary vasodilating effect of long-term nifedipine, especially during stress; this results in the improvement of the performance of the right ventricle without harmful effect on the blood gases. However, these results should be interpreted with caution on account of the small number of patients, the large interindividual variations and the absence of a reference population.

The efficacy of orally administered propafenone in the prevention of paroxysmal supraventricular dysrhythmias (atrial fibrillation, atrial tachysystole, reciprocal tachycardia) resistant to Vaughan-Williams class Ia drugs was investigated in 10 patients. Propafenone controlled dysrhythmia very well in 4 out of the ten patients, and satisfactorily in another one at a dosage ranging from 450 to 900 mg/day in 3 or 4 divided doses; this result was documented using continuous 24 hr. Holter ECG monitoring. Among the 5 clinical failures, 1 patient had atrial fibrillation primarily at night, and another poorly tolerated this agent which led to interrupt therapy.

Two case-reports of thrombopenias induced by pentosane polysulfate (PSP) are reported. PSP may play a direct role in the genesis of the thrombopenia appearing between the 5th and 15th day of treatment, or a sensitizing role where the thrombopenia occurs quite rapidly following heparin treatment. The clinical complications are haematomas, arterial or venous thromboses and haemorrhages. The platelet aggregation test is always positive in the presence of PSP. The immunological origin is probable. Monitoring of the platelet count is recommanded with this treatment.