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  Case Studies from our 1st 100  Patients 

  #1 When all of your bypass grafts close down -ME

   #2  Angina following two bypasses is two months - LF

   #3  When its your money that we’re spending - JK

   #4   Saying good-bye to seven years of chest pain - JF

   #5   When two of your grafts close down in 6 months - CW

   #6   Angina following PTCA, Bypass surgery, Rotablation & Stent Placement- JR

   #7   Single Vessel Occlusion with Refractory Angina - WY

   #8   Failed Angioplasty & Post-bypass chest pain - TO

   #9   Post-bypass refractory angina - MW

   #10 EECP when PTCA isn’t possible - JC

   #11 Better than a Heart Transplant - CS

   #12 EECP for post bypass painless ischemia - NS

   #13 When an 84 year old patient prefers a non-invasive approach -GP

   #14 EECP for post-Atherectomy restenosis - DB

   #15 EECP when two arteries are occluded - LP

   #16 When bypass surgery isn’t possible - HP

  #1 When all of your bypass grafts close down -ME

    Bypass grafts can’t last forever. As medical scientists we know this. But as a doctor, and as a person, you sure feel bad sending a patient to surgery, then discovering one year later that all of his bypass grafts have closed down. As the patient, you don’t feel so hot yourself. Such was ME’s predicament.

    ME experienced a heart attack in mid ’91. We got to work on risk factor reduction, and on minimal medication ME could carry out desired activities without much pain. Angina flared up in late ’97. ME’s stress echo returned abnormal and we proceeded with a heart catheterization. The Left Main Coronary Artery (Left Main) contained a significant but not critical 50% narrowing, compromising blood flow to the front and side walls of ME’s heart. A similar, 50% obstruction was seen at the midpoint of the Right Coronary Artery (RCA), which serves the back wall. The Left Main divides into The Left Anterior Descending (LAD), which provides blood to the front region of the heart, and the Circumflex (Circ), which serves the side wall. ME’s LAD was clear, but his Circ contained a critical, 90% narrowing. ME’s entire heart was in jeopardy. Too many blockages were present to allow safe angioplasty, and medication alone was not going to get the job done. Bypass surgery seemed to be the way for ME to go, and that was my recommendation.

    ME did well with surgery. Three grafts were placed and ME was soon able to resume his prior activities. ME noted recurrent pain in the fall of ’98. His stress test was abnormal and ME and I found ourselves back in the cath lab. His native arteries had changed only slightly. The Left Main looked a little better while the RCA was just a little worse-no surprises here. What was a surprise, actually a disappointing shock, was to see that all three of ME’s bypass grafts had closed down. Just one year out from bypass, and ME was back to square one.

    So what were we going to do? Repeat bypass was considered, but if surgery didn’t hold the first time, could we feel comfortable that the grafts would stay open following a second procedure? Also, we know that the risks of surgery are always higher the second time around. This time ME and I took a noninvasive approach. We redoubled our efforts at risk factor reduction, and ME began a course of EECP. 44 hours of EECP were carried out, finishing in early Feb ’99. ME’s angina fully resolved. ME has resumed his prior activity level; his stress echo has returned to normal and chest pain has not recurred. Too bad I didn’t get it right the first time.

    LF knew her way around the hospital cardiovascular unit. That’s what happens when you undergo three heart catheterizations, one angioplasty/stent procedure, and two open heart surgeries, all in the space of two months. Two months after her second bypass LF was still experiencing rest angina, so she also knew a lot about chest pain.

    LF came into the hospital in mid Aug ‘98 with new onset angina. Angiography was carried out the following day, revealing a 90% narrowing at the origin of  LF’s Left Anterior Descending (LAD). This obstruction, referred to as a proximal narrowing, compromised blood flow to the entire front wall of LF’s heart. The Right Coronary Artery (RCA), which supplies the back wall, was intact, as was the Circumflex (Circ), which provides blood to the side regions. The Left Main Coronary Artery (Left Main), the short but critically important vessel which gives off the LAD and Circ, thus regulating blood flow to 2/3rds of the heart muscle, contained only a mild, non-flow restrictive narrowing. Chest pain occurred during LF’s angiographic study and responded poorly to IV Nitroglycerin. An Intra-Aortic Balloon Pump (the invasive equivalent of non-invasive EECP) was inserted to provide internal counterpulsation, but LF’s chest pain persisted. This was indeed a crisis situation; some form of revascularization was clearly needed. Angioplasty was considered, but for two reasons LF’s doctors felt that bypass surgery would be a surer and safer course to take. The post-angioplasty restenosis rate of proximal LAD narrowings is 40%, but of more concern was that the trailing edge of the angioplasty balloon would have to be inflated within the Left Main, potentially "roughing up" its non-obstructive narrowing into an obstructive one, making a bad situation worse. Bypass surgery was carried out on an emergent basis, involving placement of a Left Internal Mammary Graft (LIMA) to LF’s LAD. Surgery went well, but that night LF’s EKG changed, suggesting dysfunction of the LIMA bypass graft. LF was taken back to the operating room, were fortunately the LIMA graft was found to be intact.

    LF’s recovered well from her two urgent surgeries, but three weeks later chest pain recurred. Repeat angiography demonstrated a 90% narrowing in the LIMA graft. The 90% LAD narrowing was unchanged, so LF was back where she started from. This time LF’s doctors dilated and stented the LAD narrowing, and she left the hospital angina free.

    LF was back three weeks later. Angina had recurred, and angiography, LF’s third in six weeks, showed what nobody wanted to see. The LAD Stent site had restenosed, and the Left Main narrowing had been roughed up into a flow restrictive 80% narrowing. The first diagonal branch of the LAD had similarly developed a 70% obstruction. LF’s initial single vessel disease was now Left Main and multivessel disease. Repeat bypass surgery was carried out to address this crisis situation. Vein grafts were placed to LF’s Circ and Diagonal arteries, but LF’s LAD was found to be too small to accept a vein graft. Thus LF’s second surgical bypass, while absolutely necessary, did not provide her with complete revascularization.

    Despite medical therapy, LF continued to experience angina. Her doctors advised her to cut back on her activity level, and to "learn to live with the pain". They didn’t tell her about EECP, but one of LF’s nurses did.

    In mid-Jan ’99, when I first saw LF, she was experiencing five episodes of angina per week, with occasional episodes of rest pain. Her EKG and cardiac echo exams revealed evidence of an incomplete heart attack involving the front wall, the area served by the LAD. With stress testing, LF was able to walk for 7:48. Chest pain occurred, along with a further worsening in front wall pumping function, consistent with poor flow through the non-bypassable LAD. I didn’t think that a fourth heart cath would help LF. The cardiology literature tells us that 80-90% of patients with post-bypass one or two vessel disease respond well to EEP, so I was pretty sure that LF would. LF was getting tired of all this chest pain, so she agreed to give EECP a try. LF adapted well to EECP, and began to feel better during her second week. LF could walk a mile, at 3 MPH on her treadmill, by the fourth week, and when we were finished LF was pain free. With repeat stress testing, LF walked for 10:00. Chest pain did not develop, and pumping function in the LAD distribution didn’t decrease, instead it improved. LF got her life back. EECP helped LF "learn to live without chest pain", and we were glad to have helped.

#3 When its your money that we’re spending - JK

    Cost effectiveness seems to be the watchword in health care today, and well it should be. If treatments A and B are equally safe and effective but A is less expensive, than its use should be encouraged and treatment B phased out. Cost effectiveness has a more direct meaning for JK. JK works for himself and pays his own health care bills. To JK cost effectiveness means that he must cover the cost of his treatments, and then hope that they will be effective for him. Bypass surgery in ’96 set JK back $50,000. So when chest pain recurred in late ‘98, we needed a solution to JK’s problem that was medically effective and cost-effective.

    JK experienced a moderate sized heart attack in the fall of ’96. Chest pain recurred four days later, leading to a heart catheterization. JK’s heart attack was found to be due to occlusion of his Right Coronary Artery (RCA), with resultant damage to the back wall of his heart. High grade narrowings were present in the Left Anterior Descending (LAD) and its two major branches, the Diagonals, compromising blood flow to the front of JK’s heart, and in the Circumflex (Circ) and its major branch, the Marginal, compromising flow to the side wall. Medical therapy alone would not provide JK adequate protection and there were too many blockages present to allow safe angioplasty. Our recommendation to JK was that he undergo bypass surgery.

    The Radial artery was removed from JK’s wrist and used to bypass the Marginal and both Diagonal arteries. A segment of leg vein was used to revascularize the RCA, while a Left Internal Mammary Artery (LIMA) graft was placed to the LAD. JK’s recovery from surgery was uneventful and he was soon back to work. Mild diabetes was noted and addressed with a combination of dietary modification and nutritional supplementation. In May ’97 JK passed his stress echo test with flying colors, walking for 9 minutes.

    Things went well until the fall of ’98, when JK began to notice recurrent symptoms; chest pain was occurring about once a day. With stress testing, angina occurred at five minutes and we had to stop the test at eight. The echo images demonstrated a deterioration in heart pumping function with exercise, pointing to occlusion of one of JK’s three grafts, most likely the radial artery graft. So what were we going to do? JK wasn’t enthusiastic about another heart cath. He couldn’t afford to take two months off work to recover from a second surgery - he was still paying for the first one! I also wasn’t enthusiastic about putting JK through another heart cath, as what would we do with the results? A second bypass was probably out of the question. The risks would be high and most of the vessels that could serve as bypass grafts had already been used. Angioplasty might be a possibility, but if the radial artery graft was the culprit, as I suspected, then three branch vessels would have to be dilated, and we know from research studies that multivessel angioplasty just doesn’t hold up well in diabetic patients. The literature also tells us that patients with recurrent blockages following bypass do just as well, if not better with EECP, compared to patients who have never been bypassed. It made more sense to me to omit the heart catheterization, an expensive procedure which in JK’s situation would likely not alter our therapy, and instead to begin JK on a course of EECP.

    35 hours of EECP were carried out, and while undergoing EECP JK was still able to work. After 15 treatments he noted a 70% reduction in angina. After 35 we repeated his stress echo. JK’s exercise time had increased from eight to nine & ½ minutes; this time angina did not occur, and JK’s exercise EKG and echo images both returned to normal. Now six months out from EECP, JK experiences angina only rarely. The heart catheterization that we thought our way out of would have cost around $8,000; angioplasty comes in at around $18,000, and repeat bypass procedures run in the $50-70,000 range. EECP cost JK $3,500. In JK’s situation, what I felt to be the medically best approach, also turned out to be the cost effective approach. So if treatments A and B are equally safe and effective, and A is less expensive...

#4 Saying good-bye to seven years of chest pain - JF

    Good-byes are hard to say. As teenagers, our hearts were shattered when cupid let us down, allowing our girlfriend or boyfriend to break up with us. At the end of high school, how could we say good-bye to our dearest friends? Walking our daughter down the aisle and giving her away to her handsome young man will bring every father to tears. Its hard to say good-bye to something that’s been with you for a long time. Well, not always. JF had absolutely no trouble saying goodbye to 7 years of angina. Newly married, she had things to do, things she hadn’t been able to do because of chest pain.

    Diabetes, hypertension, and a difficult to control cholesterol abnormality took their toll 7 years ago. In quick succession, JF sustained heart attacks involving the front and back walls of her heart, followed by five vessel bypass surgery in ‘93. The operation went well, but JF continued to experience angina. Repeat angiography in ’94 revealed occlusion of the three veins grafts to the Circ and RCA. The LIMA arterial graft to the LAD was patent, but the LAD itself was occluded beyond the insertion site of its LIMA graft, partially negating its value. The vein graft to the occluded Diagonal looked good, but JF didn’t feel good, with only one of her five grafts functioning as it should. There were no narrowings that could be safely approached with angioplasty, and the senior heart surgeon in Toledo felt that repeat bypass would be too risky; doctors at the Cleveland Clinic concurred. Medications were continued, and JF just got used to having chest pain.

    JF and I started working together in mid’95. Medications were continued, but we also focused on risk factor reduction, hoping to prevent any worsening of JF’s underlying coronary disease. Elevations in lipoprotein (a) and homocysteine were identified and addressed, and JF kept working hard on blood sugar and cholesterol control. JF’s interest in nutritional medicine matched my own, and we covered as many bases as we could. With these measures JF got a little better. She could do what she needed to do, but angina never really left her. Instead it became like an old friend; not a dear old friend, but more of a nagging old friend who you really don’t want to see any more.

    Periodically JF would experience flare ups of chest pain, and more than once I got nervous and tried to talk her into another heart cath, but each time JF would wisely refuse. After all, if repeat bypass or angioplasty weren’t possible in ‘94, why would they be later? Sound reasoning, but sort of difficult for an invasive cardiologist like myself to grasp.

    Illness struck the mothers of both JF and her husband in early ’99, and later that spring they both had to say their unpleasant good-byes. JF’s sister was having trouble battling a chronic disease, and these stresses flared JF’s angina to an intolerable level. I became concerned that new blockages had developed in JF’s two remaining grafts, and twisted her arm into another heart catheterization. The procedure went well. The good news was that our risk factor reduction measures had worked; JF’s arteries hadn’t worsened since ’94. The bad news was that there still wasn’t any possibility for repeat bypass. This time JF wasn’t sent for a second opinion at the Cleveland Clinic, because the Clinic doesn’t have EECP, the technique that I felt offered JF the best chance of pain relief, with the lowest treatment related risk. JF’s insurer approved her for EECP, and we got to work in March. JF adapted well to EECP. Angina began to decrease during her second week. At four weeks JF found she could do housework without experiencing fatigue. Given the severity of JF’s coronary disease, we extended her program from the usual 35 to a total of 44 hours, and by May JF was exercising on a regular basis. Two months out from EECP, JF experiences angina only rarely, and only related to stressful events. Effort induced angina doesn’t occur anymore. Seven years of angina all but went away, and for the first time in a long time JF feels truly alive. JF didn’t have any trouble saying good-bye to this old friend.

 #5 When two of your three grafts close down in 6 months - CW

    Statistics tell us that only 15-30% of bypass grafts will close down the first year following surgery. Well, someone else must be doing really well, as both of CW’s vein grafts closed down in six months. CW has never experienced angina. Diabetes has numbed the pain nerves leaving his heart, so when coronary blockages impair blood flow to CW’s heart muscle, he will experience an "anginal equivalent", in CW’s case a sensation of shortness of breath with effort. CW was experiencing a lot of shortness of breath in the fall of ’97. Moderate physical activity left him breathless. A stress test returned abnormal, and angiography revealed high grade blockages in all three of CW’s arteries. Bypass surgery was recommended, and in Feb’98 a LIMA arterial graft was placed to CW’s LAD, along with vein grafts to the RCA and Circ. Surgery went well but CW didn’t feel a whole lot better. Shortness of breath returned in the spring of ’98, and then CW felt worse. A repeat heart cath in July’98 showed what nobody wanted to see; the LIMA graft remained patent but both of CW’s vein grafts had closed down. CW’s heart pumping function remained unimpaired; early collaterals had developed from the LAD to the Circ and RCA, preventing a heart attack. Repeat bypass surgery risked damaging CW’s lifeline, the LIMA to LAD graft, and angioplasty wasn’t felt to be possible. CW was advised to continue with medical therapy. This didn’t work. Activities of daily living left CW short of breath. CW’s kidney function had worsened after this second heart cath, aggravating the ankle swelling that had troubled him since bypass surgery in Feb.

    CW toughed it out; after all his doctors hadn’t given him any other option. In late ’98, CW heard about our EECP program, not from his cardiologist, but from a friend who had benefited from EECP. Our initial workup revealed elevated levels of homocysteine and lipoprotein (a), important causes of coronary disease that had never been addressed, so we addressed them. A repeat heart cath didn’t make any sense and risked compromising CW’s kidney function further. Nutritional therapies that have been shown to help control coronary insufficiency were added, and CW began EECP. CW also had moderate vascular disease in the arteries serving his legs, making it a little difficult for us to augment his diastolic blood pressure with the external cuff inflations. For this reason we extended CW’s program to 45 hours. CW wasn’t complaining. CW was too busy walking. CW was too busy shopping. CW was too busy smiling and doing all the things he hadn’t been able to do over the past 18 months. With one good graft to work with, we can help nearly all people with recurrent blockages following bypass, and I’m glad we could help CW.

  #6 Refractory Angina despite PTCA, Bypass, Rotablation, & Stent Placement-JR                               

    I’m quite familiar with JR’s cardiac history; that’s what happens when you work with a patient through 5 heart caths, bypass surgery, and 3 angioplasty procedures, all in the space of 4 years. JR was admitted to St. Vincent’s in 2/94 with new onset angina. Angiography demonstrated a high grade LAD narrowing, involving the origin of the LAD’s diagonal branch. LAD angioplasty went well, but JR returned several weeks later with recurrent pain. Angiography showed what we didn’t expect to see: a renarrowing (termed restenosis) at the angioplasty site after only 3 weeks. This time we went with a "sure thing", and JR underwent bypass surgery, involving placement of a LIMA arterial bypass graft to the LAD.

    Chest pain recurred two months later. Angiography demonstrated the LIMA graft to be patent, but it just wasn’t providing flow to the narrowed diagonal. Medication didn’t get the job done, and JR underwent complex angioplasty of both the LAD and diagonal narrowings. We began to work on risk factor reduction and things went well for a period of time, but chest pain recurred in 11/95. Angiography demonstrated a patent LIMA bypass graft and the absence of restenosis, but a new, high grade circumflex narrowing had developed. It’s position was such that standard PTCA was not technically possible. We increased JR’s medications and his symptoms improved, but angina continued to occur at his usual activity level, and he wasn’t able to work on a regular basis. Atrial flutter, an irregular cardiac rhythm, developed in 3/97, aggravating JR’s angina and prompting admission and repeat catheterization. No new narrowings had developed since ’95, but the high grade Circ narrowing was still present. The rotoblade procedure was then available, and was used to open up and then stent JR’s Circ, with an initial improvement in symptoms.

    Chest pain recurred and angiography in 3/98 demonstrated restenosis with subtotal vessel closure at the Circ stent site. Despite four drug anti-anginal therapy, JR was experiencing chest pain with minimal effort and sometimes at rest . EECP was initiated in early April. Angina began to decrease after 12 treatments; after 20 we were able to discontinue JR’s NTG patch and decrease the Cardizem and Lopressor doses. After 35 sessions JR was in functional class 1, with a treadmill time of 10 minutes and 45 seconds.  

JR’s Comments: By the second week of EECP I could tell a difference. I didn’t have any more chest pain. I felt better and liked having my medications decreased as the treatment progressed.

Dr. Roberts’ Comments: Going into JR’s complex Circ Rotablation and Stenting procedure, we knew that the chance of restenosis was significant, but we simply had nothing else to offer him. EECP serves as an excellent alternative in complex, single vessel disease situations, allowing us to substitute a low risk, low cost, non-invasive solution for a high cost, moderate risk invasive approach.

#7 Single Vessel Occlusion with Refractory Angina - WY

    Warren Y enjoyed flying, but he had to ground himself in early ’96. "Indigestion" began to occur with progressively less exertion, prompting his internist to order a nuclear stress test. Warren could walk for only 6 & ½ minutes; the stress EKG was abnormal and the nuclear scan revealed an impairment in blood supply to the front wall of Warren’s heart. Angiography confirmed the stress test findings, demonstrating proximal occlusion of the LAD, only mild narrowings in the RCA and Circ, and normal heart pumping function. Warren’s LAD had occluded slowly, not suddenly, allowing early collaterals to grow from the RCA and Circ to the occluded LAD.

  Angioplasty was not an option. Opening up a totally occluded artery is technically difficult, and if you do get it open, it will nearly always restenose within a few months. Bypass surgery was not advisable from the risk to benefit perspective. While Warren was experiencing significant angina, he was not at risk for a heart attack (The LAD could not suddenly close off and produce a heart attack-it was already occluded and couldn’t get any worse.) As angioplasty and bypass could not be used to improve blood and oxygen supply to the front wall of Warren’s heart, the plan was to reduce oxygen demand, and with it Warren’s angina, by using drugs to decrease Warren’s heart rate, blood pressure, and force of cardiac contraction.

  Supply and demand intervention works in economics, but it didn’t work well for Warren. Tenormin lowered Warren’s heart rate to 50, decreasing angina, but robbed him of energy. The NTG patch lowered his blood pressure adequately, but produced a terrific headache. Warren was able to carry out his responsibilities as a computer programmer, but angina occurred whenever he pushed himself. Warren wanted more than fatigue, headache, and frequent angina, and we began working together in late ‘97. Warren began a program of risk factor reduction and cardiac nutritional support.  45 EECP treatments were given between 12/2 and 2/6. After 12 treatments, Warren was able to increase his daily treadmill workouts from 15 to 75 minutes. Symptoms continued to improve as Warren proceeded through EECP, and we were able to decrease and then discontinue both of his prescription medications. Now 6 months out from EECP, Warren will experience angina only if he runs following a meal. We will repeat Warren’s stress test after Warren completes his course of chelation therapy, and hopefully get him up in the air again.

Dr. Roberts’ Comments: EECP works best when there is a large blood pressure gradient between the normal vessels and the artery we which to grow collaterals to. As Warren’s LAD was totally occluded, blood pressure beyond the blockage was as low as it could go. In a totally normal artery, it is relatively easy for EECP to generate a high diastolic perfusion pressure. Warren thus had two high pressure arteries to serve as collateral sources to a single low pressure target vessel. The research available tells us that nuclear stress scans improve in 95% of patients with this single vessel disease situation, fully normalizing in 2/3rds. On the treadmill time chart, you can see that several patients increased their treadmill time by up to 4 minutes; these are typically the patients with single vessel disease, who nearly always experience a good result with EECP.

#8 Failed Angioplasty & Post-Bypass Refractory Angina - Tom O.

    I met Tom O. in mid ’97. He had had enough of drugs, angiography, and surgery and was interested in a non-invasive approach to his coronary symptoms. Tom first experienced chest pain in 6/92. Angiography demonstrated a high grade stenosis in his RCA, with 40% narrowings elsewhere. RCA angioplasty was carried out, and as you would expect, Tom’s angina resolved. What Tom and his doctors didn’t expect was that his chest pain would recur three months later. Repeat angiography demonstrated restenosis at the angioplasty site, along with a new, 80% lesion in the marginal branch of the Circ. Both arteries were dilated, and just as before, Tom’s angina resolved. Just as before, chest pain recurred a few weeks later. Both angioplasty sites had restenosed, and new blockages had developed in the LAD and its diagonal branch. Further angioplasty was not felt to be an option, and Tom underwent four vessel bypass surgery. Vein grafts were placed to the RCA, Circ, and diagonal, along with a LIMA arterial graft to the LAD. The bypass held longer than the angioplasties did, and Tom was able to stay out of the hospital for a whole six months. Severe chest pain recurred in mid ’93, prompting another heart catheterization. The marginal artery and LAD were now totally occluded, but all four bypass grafts looked good. The problem was that new 90% narrowings had developed in the marginal and diagonal arteries, beyond the touchdown site of their bypass grafts, blocking flow to the corresponding areas of heart muscle. (We call this "distal disease". A blockage is present within the grafted artery, beyond or "distal" to the insertion site of its bypass graft. Oxygenated blood flows freely through the graft, but can’t reach the heart muscle. The graft is open, but is essentially useless.) Further surgery or angioplasty was not technically possible; medications were increased and Tom’s angina decreased to a tolerable level. Tom did reasonably well between ’94 and ’96; medications were adjusted as needed, and Tom stayed out of the hospital, but he continued to experience chest pain.

    When I met Tom in mid’97, he was in functional class 3, experiencing angina at his usual activity level. The medications needed to control his symptoms were producing fatigue. A comprehensive cardiac nutritional and risk factor reduction program was initiated, and Tom began a course of EDTA chelation therapy. Tom’s insurer cleared him for EECP in the fall of ‘97, and Tom received 37 hours of EECP between 12/2 and 1/23. Tom adapted well to EECP, and we were able to cut back significantly on his medications. Over the weekend between his 17^th and 18^th treatments, Tom went deer hunting without difficulty. Tom was in functional class 1 after completing EECP, and could do more than hunt. Tom could carry out all desired activities and would experience angina only with heavy effort. We repeated Tom’s stress echo and compared it to his pre-EECP study. Exercise time had increased by one minute, angina did not occur, and we were no longer able to bring out the echo wall motion abnormalities corresponding to Tom’s known blockages. The blockages were still there, but EECP had created natural bypasses around them. While distal disease can negate the value of bypass surgery, it just isn’t an obstacle to EECP. Tom continues to do well, now 6 months out from EECP; chest pain remains minimal and we have not needed to increase any of his cardiac medications.

Tom O’s Comments: The EDTA treatments were helping me attain a greater activity level, but I still had a great deal of angina. After 10-15 EECP treatments I noticed the angina start to decrease. I now only seldom use my NTG pills.

Dr. Roberts’ Comments: After bypass surgery, 3 angioplasties, and 4 heart caths, and despite multidrug therapy, Tom was still experiencing limiting angina. A low risk, non-invasive treatment program of EECP and risk factor reduction resolved Tom’s angina, at a fraction of the cost of his prior invasive procedures. This isn’t "Alternative Medicine"; I think it is smart, cost-effective, and patient-oriented cardiology.    

#9 Post-Bypass Refractory Angina - MW

    MW was in trouble. At age 49 he had medically refractory, inoperable angina.  As his cardiologist of 7 years, I was out of ideas. MW and I first met in mid ’91. Diabetes, hypertension, and a difficult to control cholesterol abnormality had taken their toll, and MW came into St. Vincent’s with chest pain. Angiography demonstrated occlusion of the right coronary artery (RCA), with resultant damage to the inferior, or back wall of MW’s heart. High grade narrowings were seen in the remaining two arteries, the circumflex (Circ), which supplies the side wall of the heart, and the left anterior descending (LAD), which serves the front wall. It was clear that medical therapy was not going to get the job done, and MW underwent bypass surgery. Vein grafts were placed to the RCA and Circ. An arterial graft, the left internal mammary artery (LIMA,) was attached to the LAD and used to revascularize the front wall of MW’s heart. Surgery went well; chest pain resolved and MW was able to return to work and an unrestricted activity level.

    Angina recurred in early ’94. Angiography demonstrated occlusion of the vein graft to the RCA, but the other two bypass grafts looked good. Medications were advanced and MW’s chest pain resolved. MW then began a program of regular exercise, dietary modification, and risk factor reduction. By early ’96 MW was able to walk for 10 minutes on his treadmill stress test, without chest pain.

    Severe chest pain occurred in August ’96. The laboratory markers of heart muscle damage, the cardiac enzymes, were mildly elevated, consistent with an incomplete heart attack. Angiography, MW’s third, demonstrated the culprit to be occlusion of the vein graft to the Circ. The LIMA graft to the LAD was open, and collateral vessels had grown in from the LAD to the Circ. As these collaterals were providing a "back-up" blood supply to the side-wall of the heart, only a small amount of heart muscle was lost when the vein graft to the circumflex closed down. MW’s problem was that these collateral vessels were not well developed. With exercise, blood flow through these underdeveloped collaterals could not keep up with the needs of the heart muscle (It had a long way to go. Oxygenated blood in the large artery that supplies the left shoulder and arm enters the LIMA bypass graft, travels down to the LAD, and from there via collaterals to the Circ), and angina developed. Repeat bypass ran the risk of damaging MW’s "life line", the LIMA graft to the LAD, and was felt to be too high a risk

    In the fall of ’96, MW began a program of cardiac nutritional support, with continued medical therapy and aggressive risk factor reduction.  Chest pain continued but was much less severe and MW was able to work without difficulty.

    Things went well until June of ’98. Chest pain flared up, and couldn’t be controlled with drug therapy. Angiography showed, as expected, occlusion of the vein grafts to the RCA and Circ. The LIMA to LAD graft remained open, and the problem remained the inadequate collateral flow from the LAD to the Circ. As in ’96, further surgery was just not felt to be an option. MW was experiencing angina with minimal effort and sometimes at rest. I was out of ideas. We describe MW’s 6/98 condition as class 4, medically refractory, inoperable, post-bypass refractory angina, and MW had other terms to describe it. At age 49, MW couldn’t afford to retire on disability, but severe chest pain kept him from working. I was stumped, and he was stuck.

    Our EECP machine arrived in August of ’98, and MW was one of our first three patients. MW was scared, and I was nervous. We both felt a little better when MW noted less chest pain at the end of the first week. We both felt a lot better as MW’s symptoms and exercise capacity continued to improve. We were able to cut back on MW’s medications a little, and after 44 treatments he was back at work. Chest pain did not occur during post-EECP treadmill stress testing, and MW’s treadmill time was 10 minutes, up from 7 minutes pre-EECP.

    Dr. Roberts’ comments: MW had sustained two heart attacks and undergone four coronary angiograms. Despite bypass surgery, aggressive risk factor reduction, chelation therapy, and as much drug therapy as he could tolerate, MW continued to experience chest pain. It is certainly gratifying to see MW get better with EECP.

    10/98 Update: MW experienced a mild flare-up of symptoms in the fall of ’98, treadmill time had decreased slightly to 9 minutes. This time we didn’t bother with a heart catheterization. MW received 20 hour booster course of EECP, and with this MW’s chest discomfort improved markedly. MW remains in functional class one, and feels as good as he did following his initial 44 hour course of EECP in ’97.

#10 EECP when PTCA isn’t possible - JC  

    John C. and I met under difficult circumstances in late ’89. He was unconscious and fortunately doesn’t remember a thing, but I do because John kept me up all night. John presented to the emergency room with prolonged chest pain and EKG findings of a heart attack involving the back wall of John’s heart, consistent with closure of the RCA. The heart attack had damaged John’s pacing and conducting cells, leaving him with an unstable, slow heart rate, interrupted by periods of rapid arrhythmia that did not respond well to drug therapy. John arrested several times, requiring CPR and multiple defibrillator shocks. John was intubated and placed on a mechanical ventilator. As part of his treatment I placed monitoring and pacing catheters into his right heart, and an intra-aortic balloon pump device (the invasive forerunner to EECP) into his aorta, the large artery that carries blood away from the heart. It was touch and go for awhile, but these measures did work and John made a full recovery. Angiography carried out several weeks later demonstrated, as expected, occlusion of the RCA, with damage to the back wall of John’s heart. The remaining two arteries were free of obstructive disease. John continued to improve and was able to return to work.

    Chest pain recurred 9 months later. Repeat angiography demonstrated the presence of a new narrowing within the marginal branch of the Circ, which was successfully dilated. The Circ itself contained only a non-flow restrictive 50% narrowing; the RCA remained occluded, as expected. A program of medical therapy and risk factor reduction was initiated, and these measures held until early ’96, when severe pain recurred, precluding John from continuing to work in roofing. With stress testing, John walked for 7 minutes and 15 seconds, experiencing chest pain at 3 minutes; the EKG was abnormal and the post-exercise echo images showed a further deterioration in function over the back wall of John’s heart. Angiography demonstrated that the 1990 marginal angioplasty site was patent, but that the Circ, which had been supplying collateral flow to the RCA, had closed off. The RCA itself had opened up to a 90% narrowing. John’s angina was felt to be coming from a region of still viable heart muscle in the RCA distribution, which had lost its collateral blood supply when the Circ occluded. RCA angioplasty was attempted, but the narrowing present was so irregular that it couldn’t be crossed with a balloon catheter - angioplasty just wasn’t possible. John continued to experience debilitating chest pain and had to stop working. Different combinations of medications were tried, but John got only side-effects, not pain relief.

    John received 35 hours of EECP in Jan-Feb ’98. Chest pain frequency and severity decreased dramatically, and we were able to phase out Tenormin and Ismo, leaving Vasotec on board for blood pressure control. Treadmill time improved from 9 to 10 minutes, and time to angina from 4 ½ to 7 minutes. Now 6 months out from EECP, John’s symptoms remain significantly improved and we have not needed to resume any of his prior medications.

Dr. Roberts’ Comments: John’s case study illustrates the importance of collateral flow. John’s RCA had been occluded for nearly 10 years, but angina in its heart muscle distribution occurred only after the vessel proving it with collateral flow had closed off. Whenever collaterals are important, EECP should be effective. Had EECP been available in ’96 we wouldn’t have put John through a technically difficult PTCA attempt. We would have gone straight to EECP, a non-invasive, low risk, and much less expensive approach. 

    CS always enjoyed mowing her lawn, but she just couldn’t do it anymore. She couldn’t cut two rows of grass, carry laundry up the steps, or bring in the groceries. Activities of daily living, efforts that CS previously took for granted, were now producing chest pain. Medications were no longer getting the job done, and her personal cardiologist and nationally known interventional cardiologist were out of ideas.

    CS experienced a small heart attack in 1991, followed soon after by two vessel angioplasty. Unfortunately, both arteries renarrowed, necessitating placement of bypass grafts to both vessels. Chest pain flared up in ’96 but responded well to medical therapy. Symptoms returned in early ’98. An adenosine cardiolite study in 3/98 showed that CS had sustained a 2^nd heart attack, somewhere between ’91 and ’98, and demonstrated additional heart muscle was at risk. CS was placed on a comprehensive anti-anginal drug program by her personal cardiologist, but chest pain persisted, prompting referral to a nationally known interventional cardiologist at Beaumont Hospital in Detroit.

    Angiography revealed occlusion of both the Right Coronary Artery (RCA) and its vein graft, compromising blood flow to the back wall of CS’s heart. The Left Anterior Descending (LAD) and its Left Internal Mammary Arterial graft (LIMA) were also closed, eliminating normal blood flow to the front wall. The Left Main coronary artery, which controls flow into the LAD and Circ (Circumflex Coronary Artery, which supplies the side wall of the heart), contained a 50% narrowing. Fortunately, the Circ was still intact, and gave off collaterals to the LAD and RCA. So while two arteries and their grafts had closed off to produce two heart attacks, the still open Circ was providing collateral flow to both the RCA and LAD systems, and overall heart pumping function was only moderately impaired.

    Repeat bypass wasn’t possible, as the LAD and RCA were both too narrow to accept another round of bypass grafts. The Left Main narrowing could not be addressed with angioplasty, as the process of inflating the angioplasty balloon would deprive CS’s heart of its only supply of blood and oxygen. Continued medical therapy was recommended, with the option of heart transplantation should CS begin to experience rest pain refractory to drug treatment.

    At this point CS’s cardiologist learned about our program and referred her for an EECP evaluation. With only the Circumflex artery to work with, itself compromised by the 50% Left Main narrowing, I was initially concerned that we wouldn’t be able to transfer a collateral producing pressure wave into CS’s heart. But given the safety of EECP, and the fact that CS had no other good options, CS, her cardiologist, and I all felt that we should give EECP a cautious try. We’re glad we did.

    CS adapted well to EECP. She noted an increase in stamina during her second week. Chest pain began to lessen the third week. As EECP continued, CS found that she could do more and more before angina developed, and she began a treadmill workout program. Given the extent of CS’s coronary disease, she received 44, as opposed to the usual 35 hours of treatment. During weeks 8 and 9 CS returned to her prior activity level, and didn’t experience any angina. With periodic rest brakes, CS found that she could mow the lawn ( front and back) without major difficulty. We’re not thinking heart transplant anymore.

#12: EECP for post bypass painless ischemia - NS