Deans' stroke musings: Mitigation of calcium channel blocker-related oedema in hypertension by antagonists of the renin

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, June 13, 2016

Mitigation of calcium channel blocker-related oedema in hypertension by antagonists of the renin–angiotensin system

Three weeks after stopping my amlodipene for high blood pressure the swollen left ankle is still there. Right ankle(good leg) never swelled up. I wasn't warned about edema when I started taking the drug. Now on nifedipine.

I'll have to see what my doctor can do about this.

Mitigation of calcium channel blocker-related oedema in hypertension by antagonists of the renin–angiotensin system

A de la Sierra¹

¹University of Barcelona, Barcelona, Spain

Correspondence: Dr A de la Sierra, Hypertension Unit, Department of Internal Medicine, Hospital Clinic 170-Villarroel, Barcelona 08036, Spain. E-mail: ASIERRA@clinic.ub.es

Received 23 July 2008; Revised 8 November 2008; Accepted 24 November 2008; Published online 15 January 2009.

Top

Abstract

This review is aimed at examining calcium channel blocker (CCB)-related oedema and how this can be attenuated through the use of agents that inhibit the renin–angiotensin system. CCBs are effective antihypertensive agents, but their propensity for causing oedema may reduce compliance. A review of the literature has indicated that the absolute incidence of this side effect is difficult to determine because reported rates vary widely, a factor that may stem from differences in the surveillance technique (active vs passive). In a recent trial incorporating active surveillance, 25% of patients who received amlodipine 10 mg per day experienced oedema. CCB-induced oedema is caused by increased capillary hydrostatic pressure that results from preferential dilation of pre-capillary vessels. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) cause post-capillary dilation and normalize hydrostatic pressure, and are thus ideally suited for prevention/reversal of CCB-induced oedema. The efficacy of this strategy was proven using both subjective and objective techniques. ARB/CCB and ACEI/CCB combination therapy is also more effective than CCB monotherapy in controlling blood pressure. These combinations represent an important advance in the management of hypertension.