Atherosclerosis, large arteries and cardiovascular risk by Michel E. Safar, Edward D. Frohlich

By Michel E. Safar, Edward D. Frohlich

This ebook provides the present considering foreign specialists concerning the underlying mechanisms of cardiovascular possibility in addition to the pathogenesis and pathophysiology of impaired huge arterial stiffness and diminished huge arterial distensibility. It additionally demonstrates the explanation for the current method of the administration and therapy of hypertensive ailments and atherosclerosis. The special readership contains simple scientists in vascular body structure in addition to physicians and scientists in cardiovascular medication, diabetes mellitus and renal illnesses.

Show description

Read or Download Atherosclerosis, large arteries and cardiovascular risk PDF

Best cardiology books

The Official Patient's Sourcebook on Restrictive Cardiomyopathy

This publication has been created for sufferers who've determined to make schooling and examine an essential component of the therapy strategy. even though it additionally provides info helpful to medical professionals, caregivers and different overall healthiness execs, it tells sufferers the place and the way to appear for info masking nearly all subject matters on the topic of restrictive cardiomyopathy (also cardiomyopathy - restrictive; infiltrative cardiomyopathy), from the necessities to the main complex parts of study.

Brain Protection in Cardiac Surgery: Volume 1

Mind damage continues to be the most dreaded issues of cardiac surgical procedure. the variety of harm is wide; whereas a stroke could be simply outlined and clinically determined, extra sophisticated accidents most likely take place. There is still debate as to how those are clinically determined and there's a loss of general definitions permitting inter-study comparability.

Basis and Treatment of Cardiac Arrhythmias

This e-book comprises the main up-to date info with regards to mechanisms and therapy of cardiac arrhythmia. the various subject matters mentioned during this textual content mirror very lately undertaken examine instructions together with genetics of arrhythmias, cellphone signalling molecules as strength healing objectives and trafficking to the membrane.


The 1st variation of this instruction manual seemed precisely twenty-five years in the past. because of huge, immense adjustments within the quarter of diuretics, the second one variation has needed to be thoroughly revised. gigantic growth has been made within the sensible anatomy of the kidney and within the options of the way ingredients and ions are particularly transported around the numerous nephron segments.

Additional info for Atherosclerosis, large arteries and cardiovascular risk

Example text

On the basis of knowledge of the types of plaques identified as causes of thrombosis (ruptured, eroded and calcific nodule plaques), the following types of plaques are suspected to be vulnerable plaques. A Plaque Prone to Rupture Retrospective pathologic studies of plaque rupture with thrombosis suggest that prior to the event, the plaque was an inflamed, thin-cap fibroatheroma (TCFA) (fig. 2E) [11–14, 18–20]. The major components of such TCFA are: plaques with thrombosis: plaque erosion lesions from two different patients showing in B a lesion with lipid pool (Lp) and in C a necrotic core (Nc) with luminal thrombi (Th).

Consequence of longstanding diastolic hypertension, as once thought. Systolic hypertension arises de novo at any age, and often preceding diastolic hypertension [6]. What is usually different from a pathophysiologic viewpoint is that the underlying hemodynamic mechanisms of systolic BP elevation and wide PP vary considerably as systolic hypertension presents itself in various clinical populations. BP Components and Risk The information conveyed by PP is fundamentally different from that conveyed by MAP, the product of cardiac output and systemic vascular resistance (SVR).

Aldosterone administration reversibly increases rat aortic stiffness and fibronectin content in dose-dependent Izzo /Mitchell 24 fashion independent of wall stress, with no changes in collagen or elastin [33]. Arterial stiffness in humans has been related to genetic variation in components of the renin-angiotensin-aldosterone system. Variability in PWV has been related to polymorphisms in the angiotensin II receptor (AGTR1) [34, 35], while variation in PP has been related to genetic variation in the angiotensin-converting enzyme gene [36].

Download PDF sample

Rated 4.05 of 5 – based on 11 votes