Case 182a: A Brother Benefits from the Example of Case 182
Ischemic Heart Disease and Atrial Fibrillation Improved

Previous History: Born in 1933, seven years after his brother (Case 182), this man enjoyed an athletic career in both high school and college. In the fall in high school, he consumed a high caloric diet in attempts to bulk up for football while in the winter in both high school and college, he dieted and lost weight to make weight for wrestling. In college, he competed for four years in the 130 pound weight class; he stood 70 inches tall without a centimeter of fat on his body. During freshman lacrosse, he may have achieved a weight of 161 pounds. A grandmother with type 2 diabetes, who died in 1941 at 82, and a father who was a diabetes specialist led to his interest in diabetes. During the summer of 1957, he worked at a camp for diabetic children, where he was exposed to the many viruses the children harbored. In medical school, he was noted along with 10% of the rest of his class to be missing his dorsalis pedis pulses, a not uncommon finding among young people the professor of medical vascular diseases pointed out. As an intern at the Hospital University of Pennsylvania, he exercised regularly in the physical therapy department next to his on-call room and enjoyed six or seven free meals through his 18 hour work days. His weight ballooned up to 175 pounds, mostly muscle he claimed, but still a 20% weight gain over his average weight in his early 20's and a weight gain likely causing him to have the "metabolic syndrome". During his medical residencies, he ceased his muscle workouts and his weight fell back to about 160. In 1969, his cholesterol remained elevated at 257mg/dl. In the military in 1963, he underwent a glucose tolerance test because of symptoms he interpreted as reactive hypoglycemia; his one hour blood sugar was 246 mg/dl. He started on sulfonylureas in hopes of benefiting from their betacytotrophic effects, but stopped the medication as they accentuated his reactive hypoglycemia. During his endocrine fellowship, he studied the homogeneity of post-glucose load insulin levels by the density-gradient and pH-gradient electrophoretic technique. He found his own insulin peak to be delayed and small characteristic of patients with type-2 diabetes. He returned to an exercise habit and dropped his weight to 162 pounds, still a weight 12% above his average weight as a young man. His cholesterol dropped below 200 mg/dl where it has remained ever since, but his fasting blood sugar began to approach the 120's. In 1981, he again tried sulfonylureas in hopes of keeping his sugar down. He started on four daily injections of insulin which he has now taken for perhaps 24 years.

In spite of keeping his glycohemoglobin in the low to mid-5's, he lost hair on his legs in the stocking and foot areas. Still, he was able to heal many foot lesions without difficulty: splinters, blisters and minor traumas. In the early 80's, he rotated his shoe under the rotor blades of his Gravely mower as he loaded logs on the top of the mower; the blades cut through his shoe and the tops of his 1st, 4th and 5th toes leaving them macerated and bloody. He treated the toes with sterile washes, antibiotic ointment and the application of sterile Johnson & Johnson dressings. In spite of the lack of a dorsalis pedis pulse, the toes healed nicely. Perhaps because of vague chest complaints and his diabetes, his cardiologist peformed a stress test in 1982 finding a normal exercise response (to 100% heart rate based on age). In the early 2000's, he developed some numbness and discomfort in the distal feet, perhaps some neuropathy or effects of varicose veins. The persistence of reflexes, the presence of light touch and the absence of muscle atrophy or loss of balance in 2005 weighed against the diagnosis of significant neuropathy.

An awareness of his heart action led him back to his cardiologist in June, 1990. An ECHO showed mild mitral valve prolapse and an estimated ejection fraction of 79%. Electrocardiograms in February 1991 showed symptomatic heart irregularities to be due to multiple PVC's ocassionally giving a bigeminal and trigeminal rhythm. He began the daily use of aspirin for its anti-clotting effects. In March 1991, an EKG showed symptomatic palpitations to be associated with an atrial flutter-fibrillation. His cardiologist prescribed Quinaglut 325 mg and Tenormin 50mg. He proved to be allergic/sensitive to the Quinaglut dropping his granulocyte count and experiencing a rise in his hepatic transaminases. He stopped the Quinaglut. He underwent a few Long Boot treatments and returned to normal sinus rhythm. Over the next several years he had an occasional episode of atrial fibrillation that responded to what became a routine: 0.25 to 0.5 mg digoxin immediately with a 0.125mg Tenormin both to slow his ventricular rate below 120 beats/minute followed by Long Boot therapy. The Long Boot was timed initially to compress the legs on alternate beats to smooth out the irregularity of the fibrillation. When the boot rhythm appeared to be getting regular, he would change the boot monitor timing to compress his leg on every beat. Inevitably he would convert to normal sinus rhythm either in the boot or shortly after the 40 minute treatment finished.

In 1997, his office acquired a Renaissance electrical impedance apparatus allowing the beat-by-beat estimation of stroke volume and cardiac output. The following values were obtained with this apparatus:

After baseline measurements, his stroke volume and cardiac output were first measured while both legs were pumped in the Long Boot in end-diastole; his stroke volume increased 2.07-fold and his cardiac output increased 1.86-fold. His heart was then challenged by increasing afterload and pre-load simultaneously by pumping both legs during systole (initiating the leg compressions immediately after the QRS complex); his stroke volume fell to 1.1 times baseline and his cardiac output fell 5% below baseline. Minutes later, only his right leg was pumped in end-diastole; his stroke volume increased to 16% above baseline and his cardiac output recovered to 99% baseline. Again a few minutes later, both legs were pumped in end-diastole but on alternate beats: his average stroke volume rose to 35% above baseline and his cardiac output rose 13% above baseline.

In August and September 1997, he had episodes of atrial fibrillation after playing tennis and drinking alcohol, each episode converting after his routine of digoxin, Tenormin and boot therapy. He converted during the boot therapy on one episode. On the other episode his heart merely slowed and became asymptomatic. He repeated the boot treatment and converted in the boot.

In 1998, he attempted to avoid the episodes of atrial fibrillation and their rapid rates by taking digoxin and Tenormin daily. He tested his exercise tolerance wearing a Q-Med Holter monitor and documented 2 episodes of RST depression associated with vigorous exercise: one with 2mm depression lasting 3 min 39 secs and the other lasted 13 minutes 86 seconds. However, his baseline EKG revealed significant bradycardia (39) leading him to discontinue the digoxin. He consulted his cardiologist who performed an ECHO cardiogram which was read as showing borderline prolapse of post mitral valve leaflet and mild tricuspid regurgitation. The cardiologist agreed to the discontinuation of the digoxin and wondered if the RST changes on the Holter were due to the digoxin. So the Holter examination was repeated a week later; again 2 episodes of significant RST depression were seen after exercise.

The year 1999 was more of the same. On January 11th, the Holter showed 2 episodes of RST depression associated with exercise and likely hypoglycemia, one lasting 1:55 and the other 0.57 minutes. Laboratory values in February included Cholesterol 161, HDL 43, LDL 98, Tg 98 TC/HDL 3.7. He was on no anti-lipid medication having suffered some leg pains with a trial of Lipitor. On February 10th, he again developed atrial fibrillation while playing tennis and experienced modest heaviness with the rapid pulse (no discomfort prior to the tachycardia). He again took digoxin 0.5mg, Tenorminin 25 mg and an hour booting. However, his heart rate merely slowed and the AF persisted through the night. He took another 0.25 mg digoxin at 2AM and underwent another boot at 5AM and converted back to NSR at 8AM. He again started taking Lanoxin 0.25 mg qAM and Tenormin 25mg qPM. On the 12th of February, his Holter Q-Med monitor again showed 1 mm RST depression elicited by vigorous exercise on a Nordic track over 10-15 minutes. The digoxin did not prevent atrial fibrillation. On May 17th, he experienced a feeling of "worms" in his chest while holding his Gravely mower to the side of a hill. He converted to normal sinus rhythm while walking to his office for boot treatment. His blood pressure was found to be elevated (165/90) leading to an increase in his medication to Tenormin 0.25mg at bedtime, Accupril 10 mg BID and Lanoxin 0.25 mg daily. And again, the Holter Q-med monitor showed RST depressions with vigorous exercise due possibly to the digoxin or ASHD. On May 24th, his EKG showed a resting rate of rate 49 and again the daily use of digoxin was discontinued.

In 2000, he noted that all of his patients had an opacification in their right eyes as he viewed their retinas through his opthalmoscope; he solved their apparent problem by having an opacification taken out of the center portion of his own right lens. The year was otherwise not remarkable.

On the 3rd of February 2001 at 2 AM, he was awoken with another episode of atrial fibrillation. His blood sugar was 65 mg/dl. He took some glucose, Lanoxin 0.5mg and Atenolol 12.5 mg and went back to bed. At 6 AM an office EKG still showed atrial fibrillation. He underwent a 40 minute boot treatment and converted to normal sinus rhythm. He was able to garden the next day without difficulty. On the 17th of April, his laboratory values included cholesterol 175, Tg 160, HDL 44, LDL 99, FBS 127, BUN 19, creatinine 1.0, A1c 5.3%. He continued to monitor his heart rhythm and RST depressions with the Holter. Thus on June 20th, 2001 heavy exercise at 9:30-10:45 PM produced 4 episodes of RST depression. The exercise perhaps also produced a 12.30 AM episode of atrial fibrillation which he again treated with 0.5 digoxin and 25 mg Tenormin. His heart slowed but AF persisted so that at 5:35 AM he went to his office for a boot treatment and converted to NSR. He repaired again to his cardiologist who performed on the 28th of June a stress ECHO. The latter was read as showing a positive exercise EKG for ischemia, normal stress ECHO, slightly redundant posterior valve leaflet with borderline prolapse and trace mitral regurgitation. On July 3rd, he underwent a "High-resolution, cardiac-gated Computed Tomography" study the latter showed:

The year 2002 began with an episode of fibrillation on January 5th, which ended with the usual treatments. Up to this date, boot treatments had been sporadic and performed weeks apart to end individual episodes of fibrillation. As the Holter studies and the Gated CAT scan of the heart suggested the presence of significant coronary disease, the thesis was entertained that underlying ASHD was likely the etiology of the episodes of fibrillation. Further, the mitral valve prolapse seen in ECHO and ausculted as a click might be due to papillary muscle dysfunction associated with coronary disease. With this in mind, he began regular boot treatments in an attempt to decrease the episodes of fibrillation and improve his coronary blood flow. He booted five days a week after office hours and had a compressor installed at home for booting. On February 21st, 2002, he had a normal stress test. His mitral click had also disappeared.

His symptomatology became more difficult to interpret following an episode of shingles across his left chest and on his left arm. He then almost always had some chest discomfort. His exercise program, which included craddle-rocking on his abdomen and chest with both legs and head elevated, may have also elicited chest pain; his costochrondral joints became tender. The rest of 2002 and all of 2003 were free of episodes of fibrillation and his tennis game and indurance improved. In May of 2004 and July of 2005, he had single episodes of fibrillation again terminated in the boot. On both occasions he had gone a few weeks without booster boot treatments believing he might have achieved a maximal benefit from his treatments. As of August 2005, his compressor timers show 220 hours of use. Most of this use entails his own treatment. Six hours of the use was devoted to his wife who had episodes of fluttering associated with multiple PVC's. After her treatments, the episodes ceased and her t-wave amplitudes improved a few millimeters. The question was raised as to whether he might benefit from using the Cardiometrics ECP device in place of the Circulator Boot. Comparative treatments were accomplished as noted below:

Here the finger PPG, used by Cardiomedics to document augmentation for their ECP device, was used first for the ECP (Left rows 2-4) and then for the Circulator Boot (Right rows 2-4). The top tracings of each of the four rows is the EKG used to trigger each device.The bottom of each row is the PPG tracing. In the top row is seen the baseline PPG curve. Notice the curve is modestly narrow, the dicrotic notch is barely visible and the slope of the downstroke half way between the beginning of the upstroke is less steep than in the ECP tracings. In the ECP tracings the hump following the diacrotic notch became progressively bigger in the 2nd to 4th rows and the downstroke became progressively steeper. In the Circulator Boot curves, the peaks are more rounded and are occasionally notched. The overall CBC waveforms are thinner than the those of the ECP and the downstroke is less steep than that in the ECP. Such changes were to be expected. The ECP was activated before the end of the "T-wave" (225 msec after the QRS) and before the aortic valves had closed. The ECP compressions had a shorter duration (375 ms), exerted higher pressures on the leg and released the legs earlier relative to the next QRS complex than the Circulator Boot. With a pulse rate of 61-63 and a R-R interval of about 1.03 seconds, it is seen that the ECP pressure ended 0.43 seconds before the next QRS complex. In the case of the Circulator Boot, the pressure was released 40 ms before the next heartbeat. The late release of the pressure allows the negative pressure wave from the leg to reach the heart just as the aortic valve opens and thus more blood goes to the low pressure leg and less to the arm (a lower and narrower waveform).

The microvascular of both eyes is demonstrated to be normal. In other cases, reported here booting has helped resolve eye lesions.

Comments: Standard procedures for his man likely might have included the performance of leg and coronary angiograms and bypasses around the lesions seen on his heart scan. His lack of a dorsalis pedis pulse and his foot lesions would clearly have justified femoral arteriograms in some circles. Medicare might have paid $12000 for the boot treatments he has had. His hospitalization and procedures would have cost considerably more if they had gone well. Fortunately, many such procedures do go well. However, this patient's brother (case #182) did not fare well. Nor did one of his tennis partners who presented with episodic atrial fibrillation and underwent bypass surgery that was followed by multiple complications initially leaving him breathless and on dialysis... and later dead. And nor invasive therapies benefit a local podiatrist who developed atrial fibrillation and underwent procedures on his AV-node and Bundles of Hiss only to die shortly after the procedure. In contrast, the subject of this report has no vestige of his diabetes and a normal microvasculature (at least in the eyes). We know of no data showing that ECP decreases the incidence of heart arrhythmias. In this man, Circulator Boot therapy clearly seemed to have benefit. Why could there be a difference? We have spelled out the differences between the action of the ECP devices and the Circulator Boot (http://www.circulatorboot.com/introduction/CBCvsECP.html and http://www.circulatorboot.com/introduction/VascPhys.html). How do these differences possibly explain the difference effects in the treatment of atrial fibrillation? In this patient, exercise seemed to have a role in precipitating his episodes of fibrillation. Arterial hypertension and myocardial changes due to ischemia may have accompanied the exercise. Diminished ventricular emptying may have resulted in back pressure on the left atrium and dilatation of the atrial chamber. A dilated ischemic atrium may permit the single atrial contraction to change to a circus movement and atrial fibrillation. The Circulator Boot has a monitor designed to anticipate the time of the next QRS in atrial fibrillation (Dillon RS: Optimizing external cardiac-assist compressions in patients with atrial fibrillation by anticipating the next beat. Angiology 47: 123-129, 1996). Further, The Circulator Boot decreases afterload throughout ventricular systole allowing stroke volume to significantly increase and likely easing atrial emptying and decreasing atrial dilatation. In contrast, the ECP in seeking to augment the height of the dicrotic notch and in beginning leg compressions at high pressure in mid-systole increases terminal systolic ventricular presssure. Result: the Circulator Boot may terminate atrial fibrillation while the ECP does not. Until a series of patients with atrial fibrillation are studied, the importance of these differences must remain to be said as speculative. In the meantime, this physician-patient is betting his life on the differences.