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Careful investigation reveals that while oxidant production does occur during cardiac surgery in patients with chronic ischemic heart disease, cardiac oxidative stress may not progress through membrane damage and irreversible injury.

To study the efficacy of a treatment strategy for the management of hypertensive urgencies, the authors evaluated 549 patients admitted to the emergency department. They were first assigned to a 30‐minute rest period, then a follow‐up blood pressure measurement was carried out. Patients who did not respond to rest were randomly assigned to receive an oral dose of an antihypertensive drug with different mechanisms of action and pharmacodynamic properties (perindopril, amlodipine, or labetalol), and blood pressure was reassessed at 60‐ and 120‐minute intervals. A satisfactory blood pressure response to rest (defined as postintervention systolic blood pressure <180 mm Hg and diastolic blood pressure <110 mm Hg, with at least a 20 mm Hg reduction in basal systolic blood pressure and/or a 10‐mm Hg reduction in basal diastolic blood pressure) was observed in 31.9% of population. Among nonresponders, 79.1% had a satisfactory blood pressure response to the antihypertensive drug treatment in a 2‐hour average follow‐up period. No major adverse events were observed. This treatment strategy, based on standardized rest as an initial step and different antihypertensive drugs, can be effective and safe for the management of patients with hypertensive urgencies.

In young ADPKD patients, normal levels of UACR suggest that renal interstitium is comparable to that in healthy subjects and indicate an absence of subtle atherosclerotic changes in the carotid arteries. Likewise, early renal and vascular changes may be present at UACR below the levels defined as microalbuminuria.

Objective: To determine whether angiotensin converting enzyme inhibition by perindopril can reduce cardiac transforming growth factor b1 (TGFb1) and plasminogen activator inhibitor 1 (PAI-1) and therefore control collagen accumulation in an animal model with the metabolic syndrome such as the obese Zucker rat (OZR). Animals: Male OZR (group 1, n = 10); OZR treated with perindopril (group 2, n = 10); and lean Zucker rats (group 3, n = 10). Methods: During six months, group 2 received 3 mg/kg/day of perindopril orally and group 1 and group 3 were given a vehicle. Hearts were processed for pathology studies including immunohistochemical analysis with antibodies to PAI-1, TGFb1, collagen type I, and collagen type III. Results: Group 2 had lower blood pressure (126.7 (2) v 148.6 (2.7) mm Hg, p , 0.01) than untreated OZR and had decreased cardiac PAI-1 (3.6 (0.4) v 13.5 (1.7)% of positive area/field, p , 0.01), TGFb1 in myocytes (0.13 (0.1) v 9.14 (4.7)%/area, p , 0.01) and in interstitium (19.8 (6.8) v 178.9 (27.4) positive cells/area, p , 0.01), collagen I (3 (0.8) v 13.3 (1)%/area, p , 0.01), collagen III (5 (0.6) v 9.5 (0.9)%/area, p , 0.01), and collagen I to collagen III ratio (0.59 (0.13) v 1.40 (0.15) p , 0.01) compared with untreated OZR. Conclusion: These results suggest that perindopril reduces cardiac PAI-1 and TGFb1 and ameliorates cardiac fibrosis in a rat model with multiple cardiovascular risk factors.T he association of obesity, non-insulin dependent diabetes mellitus, and arterial hypertension constitutes the well known metabolic syndrome X, which is deeply involved in the development of cardiovascular disease with deleterious consequences.1 In addition, cardiac fibrosis, one of the major factors in the development of heart failure, is highly prevalent in all the aforementioned diseases.Accumulated information supports the notion that angiotensin II has, independently of its hypertensive effect, an essential role in cardiac fibrogenesis by itself and through its action on transforming growth factor b1 (TGFb1) and plasminogen activator inhibitor 1 (PAI-1).2 3 Angiotensin II induces TGFb1, a multifunctional profibrogenic cytokine that regulates cell differentiation of fibroblast into myofibroblast.4 5 Both fibroblast and, especially, myofibroblast regulate fibrogenesis in the heart by producing collagen in the cardiac interstitium. Interestingly, cardiac myofibroblasts express requisite components of the renin-angiotensin system, including angiotensinogen, renin, and angiotensin converting enzyme (ACE), and can generate angiotensin II de novo.6 7 Moreover, angiotensin II can also induce PAI-1, which inhibits activation not only of plasminogen but also of plasmin matrix metalloproteinases (collagenases), which are involved in collagen degradation.8 Consequently, increased PAI-1 concentration either in plasma or in tissue can reduce extracellular matrix degradation, contributes to the accumulation of interstitial collagen, and leads to impaired function of the fibrinolytic system. Therefore, thrombotic e...

The kidney-heart relationship has raised interest for the medical population since its vast and complex interaction significantly impacts health. Chronic kidney disease (CKD) generates vascular structure and function changes, with significant hemodynamic effects. The early arterial stiffening in CKD patients is a consequence of the interaction between oxidative stress and chronic vascular inflammation, leading to an accelerated deterioration of left ventricular function and alteration in tissue perfusion. CKD amplifies the inflammatory cascade's activation and is responsible for altering the endothelium function, increasing the vascular tone, wall thickening, and favors calcium deposits in the arterial wall. Simultaneously, the autonomic imbalance, and alteration in other hormonal systems, also favor the overactivation of inflammatory and fibrotic mediators. Thus, hormonal disarrangement also contributes to structural and functional lesions throughout the arterial wall. On the other hand, a rise in arterial stiffening and volume overload generates high left ventricular afterload. It increases the left ventricular burden with consequent myocardial remodeling, development of left ventricular hypertrophy and, in turn, heart failure. It is noteworthy that reduction in glomerular mass of renal diseases generates a compensatory glomerular filtration overdriven associated with large-arteries stiffness and high cardiovascular events. Furthermore, we consider that the consequent alterations of the arterial system's mechanical properties are crucial for altering tissue perfusion, mainly in low resistance. Thus, increasing the knowledge of these processes may help the reader to integrate them from a pathophysiological perspective, providing a comprehensive idea of this two-way path between arterial stiffness and renal dysfunction and their impact at the cardiovascular level.

These results suggest that LDC of PER + IND can control cardiovascular damage in OZR providing an additional help in the metabolic scenario likewise.

In the population studied, Ald, PRA and Ald/PRA were significantly different among essential hypertensives, and HTP with Uni-RAS or Bi-RAS. Studies with a higher number of patients will allow exploration of the usefulness of pharmacologic aldosterone blockade in Bi-RAS, and to assess the relevance of Ald/PRA to differentiate Uni-RAS from Bi-RAS.