Case 182: One Sick Man: Bad Heart, Bad Kidneys and Two Bad Legs... Survives Ten Good Years and Still Going.

Born May 19th, 1926 this patient had led an exemplary life until he joined the Navy in 1945; then he became addicted to cigarettes. He continued to smoke until 1987 when he underwent a left carotid endarterectomy for severe carotid stenosis. A preoperative stress test showed no changes with maximal exercise. Doppler flow studies at his ankles showed strong posterior tibials but some falloff in flow in the peroneals and anterior tibials. GI x-rays showed a small hiatal hernia with intermittent gastroesophageal reflux.

In November 1989, he began to suffer chest pain suggestive of angina. While his resting EKG was normal, his stress test showed significant RST changes and was accompanied by chest pain. Much of the latter, however, was relieved by Maalox. The thallium portion of the study showed "no definite evidence of myocardial ischemia at suboptimal exercise level". Coronary angiograms showed a totally occluded right coronary artery proximally with distal flow derived from left to right collaterals. His left main coronary artery had a 50% stenosis. His left anterior descending was tortuous. His first diagonal was tight and the second had a 50% narrowing. The 2nd circumflex marginal had a 60% lesion. On November 10th, he had bypasses from the aorta to (1) D1 and thence D2; (2) to Circ 1; (3) to Circ 2; and (4) to LOA... 5 grafts. Postoperatively he was hypotensive and had atrial fibrillation and ventricular tachycardia.

A balloon pump was put in his right leg. On November 11th, his right leg was noted to be ischemic and the balloon was removed. A Gortex patch angioplasty and a thrombectomy were performed. Postoperatively, the leg remained ischemic and the calf tense and painful pointing to a compartment syndrome. Circulator Boot therapy was offered and refused by the vascular surgeon lest it cause a release of muscle protein and subsequent renal failure. The surgeon performed medial and lateral compartment fasciotomies through which the calf muscles bulged separating the skin flaps three to four inches. His urine flow subsequently did fail leading to the placement of a Tenchhoff catheter and the start of peritoneal dialysis. Recurrent episodes of ventricular tachycardia, ventricular fibrillation and supraventricular tachycardia were noted. His pulmonary congestion was monitored clinically and with frequent chest x-rays.

Over the next several days perhaps 39 shock treatments were administered to his chest to cardiovert his rhythm. His EKG showed a loss of his R-waves from V1 to V6. His heart ultrasound showed vigorous contractions of his septum with diminished to absent wall motion elsewhere. The cause of his infarction was not clear. His heart surgeon considered the possibility of antibodies to heparin having a role. The relatives of the patient included a brother MD, a son MD active in emergency room medicine, a daughter-in-law MD anesthesiologist, a son medical student and a niece intensive care RN.... all of whom followed his course with the attending physicians. The relatives raised the question of his being at risk of thromboembolic disease and suggested boot therapy at least to the left leg. On November 18th a "Sequential Ted" was ordered for the left leg. The left foot became quite painful. With his renal failure and uric acid elevation, his physicians considered gout as a cause for his pain. An arthritis consultant aspirated his foot and found no urate crystals. The heart surgeon suspected foot ischemia rather than gout and allowed the application of the Circulator Boot. The latter was subsequently applied twice daily for the rest of his hospitalization. The left leg did well. During his treatments, his heart rate and pulmonary wedge pressure commonly were noted to fall while his brachial blood pressure rose. A porcine graft was applied to his right leg. He was on a respirator for two months and in the intensive care unit three months. He began to spontaneously urinate on December 5th and several days later his dialysis was discontinued. His right leg still remained swollen and at risk of amputation. On January 5th, his surgeons allowed the Circulator Boot to be applied to the right leg. The circumference of the leg was reduced daily with the pumping and the skin edges slowly approached each other. Mobilization, ambulation and physical therapy slowly followed. He was cared for by many dedicated and capable nurses. He was followed by many physicians who played important roles not recounted here. He was discharged with the following diagnoses:

• Unstable angina
• Arteriosclerotic heart disease
• Anterioapical perioperative myocardial infarction
• Cardiogenic shock
• Recurrent ventricular tachycardia and fibrillation
• Acute tubular necrosis
• Renal shutdown
• Acute respiratory distress syndrome
• Acute compartment syndrome
• Thrombosis right superficial femoral artery
• Gram-negative sepsis
• Intestinal ileus
• Peripheral and autonomic polyneuropathy
• Sliding hiatal hernia with reflux
• Mild sleep apnea
• Marked left ventricular dysfunction
• Peripheral vascular insufficiency
• Foot drop
• S/P carotid endarterectomy

He has had regular Circulator Long and Mini-Boot therapies from 1990 to the present both to keep his legs open and to support his heart. Studies like the following were made to find the optimal timing to maximize unloading his heart:

The upper left shows a baseline pulse volume tracing of his arm. The 2nd group of blocks show his arm pulse volume when the boot is pumping during systole (Td or time delay = 0); the solid rectangles represent the time of boot compressions. Note the "well" in the pulse volume curve occurring about 0.2 seconds after boot compression and ending just before the upswing of the pulse volume curve. This "well" results from boot decompression and is shown in the other group of blocks to move progressively to the right and into the systolic waveform as the delay time is increased.

In the top right, Td is 0.3 seconds and the "well" is partially imbedded in the ensuing waveform. In the 3rd group down on the right, "flicker" has occurred (the monitor "coincidence light" is flickering on and off as the next QRS complex intermittently interrupts the compression time); the "well" is imbedded in the waveform making it seem narrow and tall. In the bottom right, 0.04 seconds have been subtracted from the "flicker" delay time in an attempt to maximally unload the moment the aortic valve is opening and lessen the workload on the left ventricle when its fibers are maximally stretched

His stroke volume and cardiac output can be demonstrated to increase considerably during boot therapy with the use if the Renaissance IQ electrical impedance apparatus. Below are his dZ/dT curves before a boot treatment, during boot therapy to one leg and during therapy to both legs:

He had hospital admissions for congestive heart failure in association with viral infections or rhythm disturbances in September 1991 and January 1992. However, associated with his boot therapies, his heart size slowly decreased and has remained smaller as seen in his followup xrays:

Other medical problems required hospitalization on other occasions. In the summer of 1999, he complained of increased fatigue. He was started on human growth hormone to correct a low somatomedin-C (insulin-like growth factor-1). His somatomedin level improved. As there was no literature to support growth hormone therapy for heart failure, the therapy was soon discontinued. His somatomedin level remained within normal range. As of January 2000, he was playing golf and traveling regularly to Bermuda, Florida and Colorado. He was active on a hospital board and in social events. In 2002, however, he began to fail. He returned from Florida in the fall with flapping neck veins, slight jaundice, a hepatojugular reflux, mitral and tricuspid valvular insufficiency, cardiac enlargement and failure. He responded nicely to a course of boot therapy. Then he sought the care of his cardiologist hoping for a more permanent cure. In the next several months, he was hospitalized several times suffering syncopal episodes, 2nd degree A-V heart block (lessened with less digoxin and beta blocker), a subarachnoid hemorrhage, and insertion of a cardiac pacemaker in hopes of lessening his heart failure ($80,000 for a two-day hospitalization). The hospitalizations away from Bryn Mawr kept him away from the boot clinic. He died January 2003.

Comments: The survival of this man has been miraculous. How many such patients leave the hospital alive and how many survive a year. This man has survived ten years. One would think that if he had to do it over, he would choose to avoid heart surgery. His poor response to "Ascending Teds" should be noted. The latter are designed for the prevention of venous thrombi; they are not designed to assist the arterial circulation and they act as tourniquets in legs with low blood pressure. After these events, the man began going to church. The Lord certainly appeared to have a role in his survival. While he began to get better about the time boot therapy was commenced, he might have gotten better anyhow with the excellent care of his physicians and nurses. Booting clearly relieved the pain in his left leg. It reduced the swelling in his right leg and as the right leg improved, mention of amputation was forgotten. As noted elsewhere in these case reports, we have been able to improve kidney function with boot therapy. The role of booting in opening his kidneys is uncertain but it certainly did no harm. Finally, once he was able to return to our office gadgets, we were able to demonstrate that his booting did offer some heart support. When needed, we now follow changes in cardiac output on a beat-by-beat basis with our electrical impedance apparatus. See Dillon, Angiology 1998 in our library section.

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