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Functional but not pretty and low grade condition. See details. Be the first to write a review About this product. About this product Product Information Reflecting on the evolving concepts of hypertension over the past hundred years, "A Century of Arterial Hypertension" reveals an essential yet little-known facet of modern medicine. Put together by a team of internationally renowned experts, it is the collective work of a multidisciplinary editorial team.
Originally published in French under the auspices of the French Society of Hypertension, this English edition has been acclaimed by the International Society of Hypertension. The originality, wealth of historical documents and bibliography will make this book of interest not only to cardiologists and physicians in general, but to anyone who aspires to understand how modern medicine has achieved what it has. Additional Product Features Dewey Edition.
Measuring Blood Pressure.
A Century of Arterial Hypertension: 1896 - 1996
Metrics details. The Letter to this article has been published in Critical Care 22 Circulatory shock is a common syndrome with a high mortality and limited therapeutic options. Despite its discovery and use in clinical and experimental settings more than a half-century ago, angiotensin II Ang II has only been recently evaluated as a vasopressor in distributive shock.
We examined existing literature for associations between Ang II and the resolution of circulatory shock. Of articles identified, 24 studies including patients met inclusion criteria. Complete data existed for patients. Extracted data included study type, publication year, demographics, type of shock, dosing of Ang II or other vasoactive medications, and changes in BP, lactate, and urine output. BP effects were grouped according to type of shock, with additional analyses completed for patients with absent blood pressure.
Blood pressure as absent in 18 patients. For the patients with complete data, MAP rose by SBP rose by A total of patients with complete data were determined to exhibit a BP effect which was directly associated with Ang II. Subgroups patients with cardiogenic, septic, and other types of shock exhibited similar increases in BP. The remaining seven patients with cardiac arrest did not respond. Intravenous Ang II is associated with increased BP in patients with cardiogenic, distributive, and unclassified shock.
A role may exist for Ang II in restoring circulation in cardiac arrest. Circulatory shock is a life-threatening condition with a high risk of multi-organ failure and death and a paucity of treatment options [ 1 ]. Catecholamines and vasopressin are often required to achieve an adequate blood pressure BP , sometimes at the risk of adverse events, including peripheral and splanchnic ischemia, dysrhythmias, and organ dysfunction [ 2 , 3 , 4 , 5 ].
To date, no specific vasopressor has been shown to improve outcomes [ 6 , 7 , 8 ]. A meta-analysis by Zhou et al. Two recent randomized controlled trials have renewed interest in angiotensin II Ang II for circulatory shock [ 10 , 11 ]. In both of these studies, Ang II was hypothesized to increase mean arterial pressure MAP in patients with circulatory shock, as an adjunctive therapy to catecholamines and vasopressin standard-of-care therapy.
Ang II is a naturally occurring octapeptide that increases BP through various mechanisms, including vasoconstriction of peripheral vessels, potentiation of antidiuretic hormone ADH and adrenocorticotropin hormone ACTH release, and direct actions on postganglionic sympathetic fibers [ 12 ]. Following its discovery in the s, Ang II has been administered to humans clinically and experimentally [ 13 , 14 , 15 , 16 , 17 , 18 ].
Considerable literature surrounds the clinical and experimental use of Ang II [ 19 ]. However, to our knowledge, no systematic evaluation has associated Ang II administration with improved BP in hypotensive states. We performed a review of all published reports of intravenous Ang II use in humans. We included full manuscripts published in English, excluding commentaries, conference presentations, duplicate reports, and animal studies.
A century of arterial hypertension : 1896-1996
Abstracts were reviewed by the same two groups of authors, who independently selected eligible studies. Disagreements on study selection were adjudicated by a fifth author LB not involved in the original literature search. The following data were extracted: study type, publication year, patient demographics, dose and duration of Ang II administration, dose and duration of other concomitant vasoactive medications, type of shock, and effects on BP, lactate and urine output UOP.
For studies reporting the use of Ang II in patients with and without hypotension, only patients with hypotension were analyzed. The search strategy utilized identified potential sources, from which 24 were selected for analysis. The search was executed by two independent groups of authors, with a fifth author as arbiter for study selection.
Included studies described the blood pressure effects of human patients with hypotension who received Ang II as part of their therapy. Individual patient data were extracted where available, allowing for standard error SE calculation. SE calculations did not include compiled data i. Results of each study were compiled and weighted according to the number of patients included in each study.
Patients with missing or qualitative data were excluded from all calculations and described elsewhere. As a sub-analysis, we explored the association of Ang II in different types of shock, including cardiogenic, distributive, and other etiologies. Additionally, we performed an analysis of patients in whom BP was reported as zero or absent, which we defined as a condition of cardiac arrest.
We performed sensitivity analyses by grading each study according to study type, and performed the original analysis for each category. After full text evaluation, another 71 were excluded.
Of the remaining 24 studies, two were RCTs, nine were case-control studies, and 13 were case reports. Details are shown in Fig. In total, patients with hypotension were administered Ang II, including with complete data. For the purposes of this analysis, some forms of vasodilatory shock, such as neurogenic and medication-induced shock, were included as other causes of shock. We performed a further analysis on all included patients to discern whether any of the observed BP effect could be associated with medications other than Ang II. Of these, patients Of the patients with complete data, Of 38 patients with cardiogenic shock, 13 had complete data.
Of patients with distributive or septic shock, had complete data. Of 90 patients with shock due to other etiologies e. Only seven of the 24 studies commented on lactate or UOP. Chawla et al. None of the case controls or case studies reported serum lactate values, but five studies did comment on UOP [ 20 , 21 , 22 , 23 , 24 ]. Both Thomas et al. Scarcity of data prevented any meaningful conclusion of the effect of Ang II on organ perfusion. Significant heterogeneity in study design and lack of a comparator in most studies prevented a thorough meta-analysis, though in 21 of 24 studies, we were able to extract patient-specific data.
Additionally, the quality of the data presented within the various studies varied widely.
While the studies did not overtly label these patients as having a cardiac arrest, we classified them as such. Among this cohort, complete data were available for 13 patients, and Ang II administration was associated with an increase in SBP of Two of these 13 patients did not have return of spontaneous circulation ROSC ; and among the other five patients with incomplete data, two were nonresponders. Seventy-one of the total of Of 71 nonresponders, four had cardiac arrest.
Thirteen patients with cardiogenic shock failed to respond to Ang II, as did six with shock of other etiologies. Administration of Ang II in patients with hypotension appears to be associated with an increase in BP. The effect was seen in patients with shock of different etiologies, including distributive, cardiogenic, and other subtypes. Ang II also appears to be associated with an increase in BP in patients with angiotensin-converting enzyme ACE inhibitor overdose and in patients on chronic dialysis. Sensitivity analyses following exclusion of ATHOS-3 and cardiac arrest patients yielded results similar to the primary analyses.
Sensitivity analyses according to the quality of studies were not substantially different, but did reflect a trend toward more robust results in poorer quality studies. As such, comparisons to other studies is challenging. Nonetheless, the catecholamine-sparing effect and BP effect in these studies are consistent with the conclusion contained herein. Ang II is a molecule innate to human physiology and, along with catecholamines and vasopressin, helps maintain BP throughout a variety of conditions.
Its widely described effects include direct vasoconstriction of peripheral vessels, potentiation of water reabsorption as part of the renin-angiotensin-aldosterone system RAAS , and interaction with other endogenous pressors catecholamines and vasopressin. It is produced via multiple pathways throughout various tissue types and has important autocrine and paracrine functions, including participation in the cellular lifecycle and immune regulation [ 42 ].
The ubiquity of Ang II, its precursors and derivatives, and its receptors underlie a complex, highly evolved, homeostatic system of BP regulation. For example, RAAS activation during longstanding cardiovascular disease increases BP to maintain perfusion, but it also potentiates cardiac remodeling to withstand this increased BP [ 43 ]. Ang II also helps regulate and maintain glomerular filtration, especially during periods of reduced renal perfusion [ 44 , 45 ]. Since its discovery in the s, Ang II has been reported in over 31, humans in studies [ 19 ].
In the mids, intravenous Ang II was administered to pregnant women for preeclampsia evaluation [ 15 , 16 ]. It has also been used in patients with a multitude of diseases, including circulatory shock [ 17 , 24 , 40 , 41 , 46 ] and ACE inhibitor overdose [ 20 , 21 , 22 ]. Results of the recently completed ATHOS-3 study have confirmed its beneficial effect and safety in patients with distributive shock refractory to conventional vasopressor therapy [ 11 ].
Importantly, Ang II has been implicated as contributing to cardiac pathophysiology. Activation of the RAAS is associated with ventricular remodeling both at the site of infarct and remotely after myocardial ischemia [ 47 ]. Ang II also increases sympathoexcitation, which leads to hypertension and other cardiovascular diseases [ 48 ], and it upregulates peptides causing fibrogenesis, chemotaxis of fibroblasts, and scar formation in the healing heart [ 49 ]. ACE concentrations within myocardial tissue correlate with tissue collagen levels, and processes like fibrogenesis may cause further ACE accumulation in areas of cardiac remodeling [ 47 ].
Due to its ability to mitigate adverse myocardial remodeling, ACE inhibition has become the standard of care for patients with congestive heart failure [ 50 ].
A century of arterial hypertension, - Nicolas Postel-Vinay - Google книги
Despite inhibition, however, patients with congestive heart failure can have elevated Ang II levels, which are associated with worse morbidity and mortality [ 51 , 52 ]. Long-term effects of intravenous Ang II on cardiovascular health are unknown. The cardiogenic shock population deserves special mention because of its exclusion from the two aforementioned RCTs [ 10 , 11 ].
Patients with cardiogenic shock may have a relative deficiency of Ang II, based on similar pathogenic mechanisms.
Notably, four of the five patients had premorbid ACE inhibitor use, while information was unavailable for the remaining patient. The profound effect seen in these five patients While exposure to angiotensin receptor blocker ARB therapy was noted in in the study by Khanna et al. In fact, the effect of Ang II on patients pre-treated with ARB therapy may be difficult to predict owing to heterogeneity in pharmacodynamics and pharmacokinetics of ARB therapy [ 56 , 57 , 58 ].