After all that, it occured to me that Procardia (nifedipine) was very likely what my internist/cardiologist put me on - very briefly - last summer in an attempt to control what we believed were vascular spasms in my chest. In short order, a little edema blew up to the point where, two months and 60 mg./day of Lasix later - along with a prescription potassium supplement - he told me that I looked like I had come in with "Elephantiasis" in the calves, ankles and feet of both legs, mud-like edema under the skin, couldn't even fit into flip flops, etc.

It took about three months for it to come down, most, but not quite all of the way. I was reminded of this tonight when I looked at the prescribing information sheet for Procardia and found this on pp. 5 - 6:

Peripheral Edema: Mild to moderate peripheral edema, typically associated with arterial vasodilation and not due to left ventricular dysfunction, occurs in about one in ten patients 6 treated with PROCARDIA (nifedipine). This edema occurs primarily in the lower extremities and usually responds to diuretic therapy. With patients whose angina is complicated by congestive heart failure, care should be taken to differentiate this peripheral edema from the effects of increasing left ventricular dysfunction.

http://www.pfizer.com/files/products/uspi_procardia.pdf

For folks with CRPS, this may have been in fly in the ointment with nifedipine. In any event, rest assured the folks at Pfizer have been on it. See, "The T- and L-Type Calcium Channel Blocker (CCB) Mibefradil Attenuates Leg Edema Induced by the L-Type CCB Nifedipine in the Spontaneously Hypertensive Rat: A Novel Differentiating Assay," Terry C. Major, et al., Journal of Pharmacology And Experimental Therapeutics, 2008 325:723–731, full text at http://jpet.aspetjournals.org/cgi/reprint/325/3/723.pdf at 723-24:

Calcium channel blockers comprise a class of powerful, well tolerated, and safe antihypertensive agents that are widely used either alone or as a key component of combination therapy for hypertension. It is unfortunate that a common adverse effect of calcium channel blockers (CCBs) is vasodilatory edema, which results in peripheral leg edema. Vasodilatory edema is related to several mechanisms, including arteriolar dilation (Hayashi et al., 2005), stimulation of the renin-angiotensin-aldosterone system (Schiffrin, 2003; He et al., 2005), and fluid volume retention (Messerli, 2002). The most widely held theoretical mechanism for this edema is a disproportionate decrease in arteriolar versus venular resistance, which increases hydrostatic pressure in the capillary circulation and drives fluid shifts into the interstitial compartment. Vasodilatory edema is common and dose-dependent with first generation CCBs such as verapamil and nifedipine (Messerli, 2002; Safak and Simsek, 2006). Once edema is present, it can be slow to resolve without intervention. A number of strategies exist to treat CCB-related edema, including switching CCB classes, reducing the dosage, adding known venodilators such as nitrates, or adding renin-angiotensin-aldosterone system inhibitors such as angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers to the treatment regimen (Messerli, 2001; Weir et al., 2001). Diuretics may remediate the edema state somewhat, but at the expense of further reducing plasma volume. Traditional measures such as limiting the amount of time that a patient is upright and/or considering use of graduated compression stockings are useful adjunctive therapies.

Unfortunately, Mibefradil (Posicor), the alternative suggested in the article, appears to have been withdrawn from the US market by Roche on June 8, 1998, due to the potential for drug interactions, some of them serious, which could occur when taken together with certain medications. http://en.wikipedia.org/wiki/Mibefradil

Perhaps Pfizer is not yet ready to concede defeat. (To be continued?)

Mike