Carotid wall inertial index increase is related to intima-media thickening in hypertensive patients.

OBJECTIVE: The aim of this study is to evaluate the relationship between carotid intima-media thickness (IMT) and arterial wall inertial behaviour. METHODS: The simultaneous and noninvasive assessment of the intima-media complex and arterial diameter waveform was performed using high-resolution ultrasonography. The common carotid artery of eleven normotensive subjects (NTA) and eleven mild-to-moderate essential hypertensive patients (HTA) were measured noninvasively using tonometry and an automatic densitometric analysis of B-mode images to obtain IMT and instantaneous pressure (P) and diameter (D) loops. A linear discrete time model was used to estimate the inertial index (K(M)) using a system modelling-identification approach. RESULTS: In NTA K(M) was 0.333+/-0.256 (mmHg x s2/mm) and IMT 0.643+/-0.061 (mm), whereas in HTA K(M) was 0.798+/-0.590 (P < 0.05) and IMT 0.760+/-0.034 (P < 0.025). When all data of K(M) versus IMT of NTA and HTA were pooled in a linear regression analysis, a correlation coefficient of r = 0.61 (P < 0.05) was obtained. CONCLUSION: Wall inertia increase was associated with a higher IMT, suggesting that the intima-media thickening might be partially related to vascular hypertrophy manifested as increase of inertial behaviour.

[Gas exchange changes in the postoperative period of heart surgery]. / Alteraciones del intercambio gaseoso en el post-operatorio de cirugía cardíaca.

We studied prospectively 59 open-heart surgical patients (CBPS) in order to evaluate postoperative arterial blood gases evolution and its predictive value of respiratory and non-respiratory post-surgical complications. Twenty-four hours after CPBS 28 over 59 patients showed left pleural effusion and/or left lower lobe atelectasis. 62.9% or pleural effusions were only blunted costophrenic angle. Chest x-ray film were normal in 38.9% (23/59) of patients. Forty-eight hours after CPBS only 5% (3/59) radiographs were normal and only 31% of pleural effusion were classified as minimal. Forty-eight hour radiographs worsened in 69.4% of the patients. (Table 1). During 48 hours period 71% of patients showed pleural effusion and 42% atelectasis. Only 1 patient showed an atelectasis up a third of hemithorax (3.5% of abnormal chest X-ray films). Twelve hours alveolo-arterial quotient (a/A) was decreased in 50/59 patients (0.51 +/- 0.16), more deeply at the second day. There was no relationship between CBP time and a/A at 12 or 48 hours. The normal chest X-ray film patients mean a/A was no different (0.54 +/- 0.17). The a/A at 48 hours was no different between patients with and without lower lobe atelectasis. Nine patients (15%) developed respiratory complications (RC) and 11 (19%) non-respiratory complications (NRC) (Table 2). There was no difference in CBP time (76.9 +/- 27.9 vs 88.1 +/- 27.7 min p = NS) nor aortic cross-clamp time (52.61 +/- 20.43 vs 59.57 +/- 19.39 min p = NS) between patients with and without RC. There were no differences in a/A at 12 hours (0.47, 0.51, 0.48 p = NS) and 48 hours (0.34, 0.32, 0.30 p = NS) between patients without complications, with RC and with NRC (Table 3). There was no correlation between 12 or 48 hours a/A and intensive care or hospital stay length. The absence of predictive value of hypoxemia could be explained from a different source of early a/A fall and important RC. It could mean that RC after CPBS are not specific of that sort of surgery nor involve mechanisms related to that special intraoperative circumstances, which is not the same for gas exchange alterations. We conclude that a/A deterioration is a very common finding after CBP and does not identify particularly risky patients.

Mechanical vs intrinsic components in the improvement of brachial arterial compliance. Comparison of the effects of atenolol versus ramipril in hypertensive patients.

The aim of this study was to compare the mechanical and intrinsic effects of an angiotensin converting enzyme inhibitor, vs a beta-blocker, on brachial arterial compliance. In a double blind study, 34 essential hypertensive patients were treated for 3 months with either ramipril 2.5-5.0 mg daily (n = 17, age 57 +/- 7 y, 11 males) or atenolol 50-100 mg daily (n = 17, age 53 +/- 8 y, 11 males). Blood pressure (BP), brachial artery diameter (D), brachial-radial pulse wave velocity (PWV) and effective compliance (Ceff), were measured before and at the end of the study. Isobaric evaluation (Ciso) was performed in the entire population studied at an average mean BP of 110 mmHg. Ramipril significantly reduced BP from 155 +/- 16/94 +/- 6 mmHg to 140 +/- 15/85 +/- 7 mmHg (p < 0.001) without affecting heart rate (HR; 74 +/- 10 vs. 75 +/- 12 bpm). In addition, it significantly improved both PWV (18%; p < 0.001) and arterial compliance (45%; p < 0.001), from which 35% was related to a pressure independent effect (p < 0.01). Atenolol also induced a reduction in both BP (159 +/- 17/96 +/- 10 to 133 +/- 13/81 +/- 8 mmHg; p < 0.001) and HR (76 +/- 10 to 57 +/- 7 bpm; p < 0.001). In a similar way, PWV (11%; p < 0.05) and Ceff (30%; p < 0.05) were significantly improved without significant change in Ciso. This suggests that blood pressure reduction was responsible for compliance improvement. In conclusion, it is suggested that atenolol induces only hemodynamic changes, mediated mainly by BP reduction. In contrast, the improved brachial buffering function observed after ramipril involves not only hemodynamic changes, but also changes mediated by other mechanisms, such as modification of wall structures.

[Vascular dysfunction in hypertension evaluated by nonivasive assessment of arterial impedance]. / Evaluacion de las alteraciones circulatorias de la hipertension arterial mediante la determinacion no invasiva de la impedancia arterial.

The effects of high blood pressure on arterial vessels has become an important topic of research. These effects can be evaluated by analyzing three major components: systemic vascular resistance, arterial compliance and wave reflection. The increase in systemic vascular resistance and arterial stiffness produces modifications of left ventricular afterload and morphologic changes of pressure and flow waves. These effects can eventually cause structural changes of the left ventricle, an increase in oxygen consumption and a decrease in coronary perfusion. Until recently, invasive methods were the only means to evaluate arterial function. The aim of this review is to assess the usefulness of non invasive methods to determine the components of arterial impedance in order to evaluate the hemodynamic changes due to high blood pressure.