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PERIPHERAL ARTERIAL DISEASE

This condition probably affects someone you know

By John Paul Runyon MD, FACC

Most people are aware that atherosclerosis can cause blockages in the coronary arteries, resulting in chest pain or heart attack, or in the carotid arteries, precipitating a stroke. But atherosclerosis can lead to another serious but often under-diagnosed condition: peripheral arterial disease (PAD). Defined as atherosclerotic obstruction of the arteries to the lower extremities, PAD causes leg pain and is associated with other cardiovascular disease. Although lower extremity PAD affects an estimated 12 to 20 million people in the United States, only 4 to 5 million of them are experiencing symptoms.

WHAT IS PAD?

Atherosclerosis is the major cause of lower extremity PAD, and its risk factors are the same as for atherosclerosis of the coronary or carotid arteries.

CIGARETTE SMOKING—More than 80 percent of patients with lower extremity PAD are current or former smokers. Large studies have found that smoking increases the risk of lower extremity PAD two- to six-fold and the risk of intermittent claudication (leg pain during walking) three- to ten-fold. Smoking is two to three times more likely to cause lower extremity PAD than coronary artery disease. The risk increases with the number of cigarettes smoked per day and the number of years a person smoked.1

DIABETES MELLITUS—Twelve percent to 20 percent of patients with lower extremity PAD also suffer from diabetes, which increases the risk of lower extremity PAD two- to four-fold. That risk is proportional to the severity and duration of diabetes.2

HIGH CHOLESTEROL—Elevated lipid levels (cholesterol and triglyceride) are associated with the development of lower extremity PAD, as are elevated total and low-density lipoproteinema (LDL) cholesterol, decreased high-density lipoproteinema (HD) cholesterol, and hyper-triglyceridemia.

HIGH BLOOD PRESSURE—Hypertension is associated with lower extremity PAD, although not as strongly as it is with cerebral vascular and coronary artery disease. Patients with hypertension are two-and-a-half to four times more likely to experience intermittent claudication.

HYPERHOMOCYSTEINEMIA—Elevated levels of homocysteine in the blood (homocysteine is an amino acid) and C-reactive protein (inflammation) are also associated with lower extremity PAD.

AGE—The incidence of PAD increases with age. PAD is present in 2.5 percent of individuals 60 years and under, 8.3 percent of those aged 60 to 69, and 18.8 percent of those 70 years and older.3 As the population ages, we’re likely to see an increase in the prevalence of lower extremity PAD. By the year 2030, 45 percent more men and 14 percent more women are expected to suffer from lower extremity PAD.

The prognosis of patients with lower extremity PAD depends on whether or not they also have coronary artery disease and cerebrovascular disease—conditions that are two to four times more likely in patients with lower extremity PAD. Among patients presenting with lower extremity PAD, approximately half to two-thirds show evidence of coronary artery disease, and approximately 12 to 25 percent have significant carotid artery disease. Approximately one-third of men and one-quarter of women with known coronary artery or cerebrovascular disease also have lower extremity PAD.

Heart attack, stroke, and cardiovascular death are also more frequent in patients with lower extremity PAD. For example, the risk of heart attack is increased 20 percent to 60 percent. The risk of death due to coronary artery disease is two to six times higher, and the risk of stroke is increased approximately 40 percent.

SYMPTOMS OF LOWER EXTREMITY PAD

CLAUDICATION—Intermittent claudication (leg pain during walking) is the most common symptom in patients with lower extremity PAD. Claudication is defined as fatigue, discomfort, or pain that occurs in the leg muscles during exertion caused by exercise-induced ischemia (lack of adequate blood flow). When claudication occurs during exercise only, with adequate blood flow restored after several minutes of rest, the diagnosis is “intermittent claudication.”

Symptoms of intermittent claudication include fatigue, aching, numbness or pain while walking, and these symptoms can be aggravated if the individual is walking uphill or at a rapid pace. Specific leg symptoms often depend on the anatomic site of the arterial blockage. For example, blockage of the iliac arteries can produce pain in the hip or buttocks in addition to the thigh and calf. Blockage in the femoral and popliteal (knee) arteries is usually associated with calf pain, while blockage in the tibial arteries (below the knee) can produce calf pain, foot pain, and numbness.

Claudication is considered mild if individuals experience little or no lifestyle limitations. Patients with mild claudication usually can walk more than 200 yards before suffering any significant symptoms. Moderate to severe claudication, however, is lifestyle-limiting. These individuals cannot walk 200 yards before experiencing symptoms. As a reference, a city block is approximately 100 yards long. Therefore, patients with moderate to severe claudication can walk less than two blocks.

CRITICAL LIMB ISCHEMIA—More severe than claudication, critical limb ischemia is limb pain that occurs at rest, or impending limb loss that is caused by severely restricted blood flow to the leg. Patients with critical limb ischemia have inadequate blood flow to sustain the leg, resulting in chronic rest pain, ulcers, and gangrene. The discomfort is often worse when the patient is in bed with the leg elevated and can lessen when the limb is lowered. The pain commonly can awaken patients from sleep and can render them severely disabled, often unable to walk. If untreated, these individuals usually require a major amputation within six months. The quality of life for patients with critical limb ischemia can be worse than that of patients with terminal cancer.

Factors that can contribute to or exacerbate critical limb ischemia include diabetes, severe congestive heart failure, infection, skin breakdown, and traumatic injury.

The majority of people with lower extremity PAD, however, do not experience symptoms. In a study of lower extremity PAD performed in Southern California, 11.7 percent of symptomatic patients showed large-vessel lower extremity PAD on noninvasive testing. The prevalence of intermittent claudication was 2.2 percent in men and 1.7 percent in women.4 Thus, the fraction of individuals with intermittent claudication (classic symptoms) dramatically underestimates the true prevalence of lower extremity PAD. Overall, symptoms were present in approximately one-fifth of the population with evidence of lower extremity PAD.

Even without classic symptoms, patients with lower extremity PAD still have systemic (generalized) atherosclerotic disease and often experience leg dysfunction, diminished functional status, and increased cardiovascular risk. In other words, even without symptoms, people with lower extremity PAD still have measurable limb dysfunction and adverse cardiovascular outcomes, and they bear the same risk factors of patients with symptomatic lower extremity PAD. (Patients with asymptomatic lower extremity PAD can also have other causes of leg pain—lumbar disc disease, spinal stenosis, sciatica, radiculopathy, muscle strain, and neuropathy.) Thus, regardless of symptom status, patients with lower extremity PAD should take steps to reduce their risk factors and seek treatment as they would for coronary artery disease.

TREATMENT OF LOWER EXTREMITY PAD

REDUCE THE RISK

To reduce the risk of heart attack or stroke associated with lower extremity PAD, lifelong treatment should include modification or elimination of the atherosclerotic risk factors.

STOP SMOKING—Studies have found that the risk of death, heart attack, and amputation is substantially greater in these individuals with PAD who continue to smoke compared with those who stop smoking. Approximately 15 to 30 percent of patients can quit smoking within a year with physician advice and drug intervention (Wellbutrin®, Nicoderm Patch®, etc.)

MANAGE DIABETES—Patients with both lower extremity PAD and diabetes should receive proper foot care, including an evaluation by a podiatrist. Skin lesions and ulcerations should be addressed urgently. Diabetic patients with lower extremity PAD should be treated with glucose-control therapies that reduce the hemoglobin A1C to less than 7 percent. Home care should include the use of appropriate footwear, daily foot inspection, and skin cleansing.

LOWER BLOOD PRESSURE—Treatment of high blood pressure reduces the risk of cardiovascular events such as stroke, heart failure, and death. In the “Heart Outcome Prevention Evaluation Study,” patients with coronary disease, cerebrovascular disease and PAD were randomly treated with ramipril (Altace®) or placebo. Ramipril (Altace®) reduced the risk of heart attack, stroke, or vascular death in patients with PAD by 25 percent.6 Therefore, ace-inhibitors should be considered as treatment for patients with lower extremity PAD.

LOWER CHOLESTEROL—Treatment of elevated lipids reduces the risk of adverse cardiac events in patients with atherosclerosis. The “Heart Protection Study” treated patients with coronary artery disease, cerebrovascular disease and peripheral arterial disease randomly with simvastatin (Zocor®) or placebo. This study included 6,748 patients with PAD and demonstrated a 25 percent risk reduction over five years.5 On the basis of these findings, it is now recommended that patients with PAD and LDL cholesterol of greater than 100 mg per dl be treated with a statin (lipid lowering drug).

BLOOD THINNERS—Patients with lower extremity PAD should be treated with antiplatelet therapy to reduce the risk of heart attack, stroke, or vascular death. Aspirin, in daily doses of 75 to 325 mg, is recommended as safe and effective antiplatelet therapy.

CLAUDICATION

A supervised exercise program is the initial treatment for patients with lower extremity PAD and claudication. Patients who walk regularly will, over time, increase the speed and duration of the walk and experience decreased claudication symptoms. Structured exercises are also likely to benefit patients who are treated with the other therapies listed below.

Drug therapy is another option for lower extremity PAD. Cilostazol (Pletal®) has been found to improve symptoms and increase walking distance in patients with lower extremity PAD and intermittent claudication in the absence of congestive heart failure.

Endovascular procedures are indicated for individuals with lifestyle-limiting lower extremity PAD with claudication. Endovascular techniques to treat peripheral arterial occlusive disease include balloon angioplasty, stents, laser, cutting balloons, thermal angioplasty, and plaque excision. Endovascular therapy for individuals with lower extremity PAD and claudication offers a high success rate, a low incidence of complications or death, and in the majority of patients, it can be performed as an outpatient procedure.

In general, surgery should only be considered after nonsurgical therapies have failed. Surgical intervention is typically reserved for patients whose impairment significantly threatens their employment or requires significant alteration in lifestyle.

CRITICAL LIMB ISCHEMIA

More than 20 percent of patients with critical limb ischemia (CLI) will die within one year, and nearly half of CLI patients require revascularization to save the limb. An estimated 220,000 to 240,000 major and minor lower extremity amputations are performed in the United States in Europe each year because of critical limb ischemia.7

This naturally mandates a more aggressive treatment approach, which should be determined on a case-by-case basis. Issues to consider include the severity of the patient’s condition, the presence of additional complications, and the arterial anatomy.

If the individual is a candidate for endovascular therapy, this strategy should be attempted first. If the patient is not a candidate for endovascular therapy, surgical revascularization can be required. Regardless of the initial treatment strategy, patients must be monitored closely.

You should discuss your individual treatment options with your personal physician.

REFERENCES

1. Price JF, Mowbray PI, Lee AJ, et al. Relationship between smoking and cardiovascular risk factors in the development of peripheral arterial disease and coronary artery disease: Edinburgh Artery Study. Eur Heart Jour 1999; 20:344-353.

2. Hiatt WR, Hoag S, Hamman RF. Effect of diagnostic criteria on the prevalence of peripheral arterial disease. The San Luis Valley Diabetes Study. Circulation 1995; 91:1472-1479.

3. Kannel WB. The demographics of claudication and the aging of the American population. Vasc Med 1996; 1:60-64.

4. Criqui MH, Fronek A, Barrett-Connor E. The prevalence of peripheral arterial disease in the defined population. Circulation 1985; 75:510-515.

5. Heart Protection Study Collaborative Group MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-rick individuals: a randomized placebo-controlled trial. Lancet 2002; 360:7-22.

6. Yusuf S, Sleight P, Pogue J, et al. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med 200; 342-145-53. Errata in: N Engl J Med 2000; 342-1376; N Engl J Med 2000; 342:748.

7. Allie DE, Hebert CJ, Lirtzman MD, et al. Critical limb ischemia: a global epidemic. A critical analysis of current treatment, unmasks clinical and economic costs of CLI. Eurointervention 2005: 1:60-69

The patient is an 80-year-old male, ex-smoker, with a history of coronary artery disease, high cholesterol, prior coronary bypass surgery, and prior aortic valve replacement. He presented with a non-healing wound on his left great toe.

John Paul Runyon is a Board-certified physician with expertise in cardiovascular medicine; significant background in clinical education and training of physicians. Vast network of peer relationships with key opinion leaders in cardiology and peripheral/endovascular medicine.

Please visit Dr. Runyon on his websites, blogs and on social media;

WEBSITES

JohnPaulRunyon.com

JohnPaulRunyon.org

JohnPaulRunyon.net

John-Paul-Runyon.com

JohnPaulRunyonInfo.com

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#Cardiologist #Cardiology

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johnpaulrunyon1960-blog · 9 years ago

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Abdominal Aortic Aneurysms: The Silent Killer

By John Paul Runyon MD, FACC

One of the leading causes of death in the United States is a condition that many people don’t even know they have. Abdominal aortic aneurysms (AAAs) affect approximately 2.7 million people in the United States, with an additional 200,000 new diagnosis each year,1 although most are asymptomatic, which makes diagnosis difficult. However, new treatments and early detection can make a difference in patient outcomes.

WHAT IS AN AAA?

An abdominal aortic aneurysm is the swelling or ballooning, of the abdominal aorta, which is the main artery that carries blood from the heart to all parts of the body. It is characterized by a gradual and/or sporadic expansion (enlargement) in its diameter. Although an aneurysm can occur in any part of the body, it is most common in the abdominal aorta.

The prevalence of AAA varies with a number of demographic factors, including age, gender, family history, and tobacco use. In general, AAAs that are 2.9 cm to 4.9 cm in diameter occur in about 1.3 percent of men and 0.1 percent of women age 45 to 54, and in as many as 12.5 percent of men and 5.2 percent of women age 75 to 84.

Patients who have undergone coronary artery bypass grafting (CABG) are three times more likely to have an AAA than those who have not. Among patients with prior CABG, men have a 6.6 percent change of developing an AA, whereas women have a 3.2 percent chance.2

Some patients may also be genetically predisposed to the formation of abdominal aortic aneurysms. First-degree relatives of patients with AAA have two to four times the normal risk for AAA.3

The three most common complications of aneurysms are rupture, thromboembolic events (stroke), and the compression or erosion of adjacent structures. Rupture is the most widely recognized complication of AAAs. Ruptured abdominal aortic aneurysms result in approximately 30,000 deaths each year and are the 17th leading cause of death in the United States. Ninety percent of patients with ruptured abdominal aortic aneurysms will die.4

SIGNS AND SYMPTOMS

Although most AAAs are asymptomatic, patients may experience abdominal discomfort and back pain, and some patients become aware of abdominal pulsations. Less-frequent symptoms include pain in the legs, chest, or groin, anorexia, nausea, vomiting, constipation, or dyspnea.

Compression of the left iliac vein can cause the left leg to swell. As the aneurysm expands and compresses vertebrae and lumbar nerve roots, pain can develop in the lower back, possibly radiating to the back of the legs. Flank pain radiating to the upper left thigh or scrotum can reflect compression of the left genitofemoral nerve. Nausea and vomiting can occur as the aneurysm compresses the duodenum (first segment of the intestine). Bladder compression can cause urinary frequency or urgency.

When rupture occurs, low blood pressure, back pain, and a pulsatile abdominal mass are the classic findings.

DIAGNOSIS AND TREATMENT

Aortic diameter can be measured accurately by ultrasound imaging. Because this method of screening can potentially catch an AAA before it ruptures, it has become the focus of population-based screening programs. The Screening Abdominal Aortic Aneurysms Very Efficiently Act (SAAVE) was included in the Deficit Reduction Act of 2005 (DRA) and signed in law in February 2006. This Act provides Medicare Part B coverage for screening ultrasound examinations to detect AAA.

Beginning January 1, 2007, Medicare began offering a free one-time ultrasound AAA screening to qualified seniors as part of their Welcome to Medicare Physical Exam (WTMPE). Men who have smoked at least 100 cigarettes in their lifetime, as well as men or women with a family history of AAA, qualify for the one-time screening once they have undergone the WTMPE. The WTMPE must be completed within the first six months of Medicare eligibility, but there is no established time frame thereafter for completion of AAA screening. Providers who perform the WTMPE physical and order the AAA screening ultrasound examination need to document the AAA Risk factor.

The Society of Vascular Surgery (SVS), however, has recommended a more aggressive screening schedule for AAA: men 60 to 85; women 60 to 85 with cardiovascular risk factors; and men and women 50 or older with a family history of AAA.

At the present time, two options exist for treatment of AAAs: open surgical repair and endovascular aneurysm repair. Open surgical repair consists of isolating the abdominal aortic aneurysm vial laparotomy (abdominal incision) and replacing the aneurysm with a synthetic graft.

The second option, endovascular aneurysm repair (EVAR), utilizes small incisions made in the femoral arteries to deliver a self-expanding graft into the abdominal aorta via a catheter-based system. The stent graft is flexible and conforms to the structure of the normal aorta above the aneurysm, preventing blood from entering the aneurysm.

The AAA stent graft remains in the patient for life and is inspected during periodic follow-up using computerized tomography angiography (CTA). EVAR has been FDA-approved for the treatment of AAAs in the United States since 1999, and it offers a reliable alternative for patients who meet the vascular anatomy and AAA location requirements.

THE INFORMED PATIENT

In choosing between open repair and EVAR, patient preference is of great importance. It is essential that the patient be well informed in making such choices. Likewise, it is not appropriate to arbitrarily set a threshold diameter beyond which elective repair should be recommended. The decision for AAA repair must be individualized in each case. The risk for rupture of small (less than 5 cm) AAA is quite low, and a policy of careful surveillance up to a diameter of 5.5 cm is safe, unless rapid expansion (greater than 1 cm per year) or symptoms develop. For women or AAAs with greater-than-average rupture risk, elective repair at 4.5 cm to 5.0 cm is appropriate.5

Abdominal aortic aneurysms continue to be a leading cause of death in the United States. Endovascular abdominal aortic repair (EVAR) has gained tremendous attention for treatment of AAA. However, early detection or screening of AAAs is an equally important issue. Despite advances in diagnostic imaging and medicine in general, there has been no change in the number of patients who present to U.S. hospitals with ruptured AAAs in the last 20 years.

Early detection can be achieved through increased patient and physician awareness, in conjunction with organized screening programs. Compelling data reveal that identification of AAAs can save lives at a cost to society that compares favorably with other well-accepted interventions.

REFERENCES

1) Kent K. Zwolak R, Jaff M, et al. Screening for abdominal aortic aneurysm: A consensus statement. J. Vasc Surg 2004; 39: 267-269.

2) Dall’olmo C, Ippolito A, Mcliduff J, et al. Incidence of AAAs in CABG Patients. Endovasc Today 2005: 4: 53-58.

3) Engtsson H, Sonesson B, Lanne T, et al. Prevalence of abdominal aortic aneurysm in the offspring of patients dying from aneurysm rupture. Br J Surg 1992; 79: 1142-3.

4) Johansen K, Kohler T, Nicholls SC, et al. Ruptured abdominal aortic aneurysm: the Harborview experience. J. Vasc Sur 1991; 13: 240-5.

5) Brewster D, Cronenwett J, Hallett J, et al. Guidelines for the treatment of abdominal aortic aneurysms. J. Vasc Surg 2003; 37: 1106-17.

Please visit Dr. Runyon on his websites, blogs and on social media;

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JohnPaulRunyon.com

JohnPaulRunyon.org

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#Cardiologist #Cardiology

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#Clamshell Proximity Card #Proximity cards #access control system

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Publications – John Paul Runyon

The following are publications that Dr. John Paul Runyon has authored and co-authored:

Laird J, Joye J, Sachdev N. Huang P, Caputo R, Mohiuddin I, Runyon J, Das T. Recanalization of Infrainguinal Chronic Total Occlusions With the Crosser System: Results of the PATRIOT Trial. J Invasive Cardiol. 2014 Oct;26(10), 497-8.Losordo DW, Kibbe MR, Mendelsohn R, Marston W, Driver VR, Sharafuddin M, Teodorescu V, Weichmann BN, Thompson C, Kraiss L, Carman T, Dohad S, Huang P, Junge CE, Story K, Weistroffer T, Thorne TM, Millay M, Runyon JP, Schainfeld R. Autologous CD34+ cell therapy for critical limb ischemia investigators. Circ Cardiovasc Interv. 2012 Dec; 5(6):821-30.

Safain RD, Niazi K, Runyon JP, Dulas D, Weinstock B, Ramaiah V, Heuser R. Orbital atherectomy for infrapopliteal disease: Disease concept and outcome data for the OASIS trial. Catheter Cardiovasc Interv. 2009 Feb 15;73(3); 406-12.

Runyon JP, “Plaque excision and stent graph deployment for SFA occlusion: A case report on this combination therapy.” Endovascular Today. 2007, February; 90-2.

McKinsey JF, MD, Ramaiah VG, MD, Runyon JP, MD, Allie DE, MD, Walker CM, MD, Garcia L, MD, Gammon RS, MD: 1 Year Results of Treatment of Infrapopliteal Arterial Occlusive Disease using the SilverHawk Plaque Excision Device. Submitted September 2005 to The Peripheral Vascular Surgery Society, for the PVSS Meeting January 27-29, 2006. Accepted.

Ramaiah V, Gammon R, Kiesz S, Cardenas J, Ruyon JP, Fail P, Walker C, Allie DE, Chamberlin J., Solis M, Garcia L, Kandzari D. Midterm outcomes from the TALON Registry: Treating peripherals with SilverHawk: outcomes collection. J Endovas Ther. 2006 Oct; 13(5): 592-602.

Maurice Solis, Stefan Kiesz, Roger Gammon, Venkatesh Ramaiah, Craig Walker, David Allie, John Runyon, Joseph Cardenas: Early Results of Plaque Excision in the Treatment of Lower Extremity In- Stent Restenosis. Accepted TCT05 Washington Convention Center, Washington DC, October 16-21, 2005.

Roger Gammon Joseph Cardenas, Venkatesh Ramaiah, John Runyon, Peter Fail, Craig Walker, David Allie, Jack Chamberlin, Maurice Solis, Lawrence Garcia, Prakash Makam, Jose Vale, Stefan Kiesz. Acute and Long-Term Outcomes for Treatment of Lower Extremity PAD with SilverHawk Plaque Excision System. Accepted. TCT05 Washington Convention Center, Washington DC, October 16-21, 2005.

Young JJ, Marcus DP, Abbotsmith CW, Broderick TM, Choo JK, Runyon JP, Schneider JR, Shimshak TM, Geier RP, Keriakes DJ. “Durable clinical benefit following Sr90 Beta irradiation therapy for in-stent restenosis in high-volume community practice.” J Invasive Cardiol. 2003 Jan:15 Suppl A:9A-13A.

Gilchrist IC, O’Shea JC, Kosoglou T, Jennings LK, Lorenz TJ, Kitt MM, Kleiman NS, Talley D, Aguirre F, Davidson C, Runyon J, Tcheng JE. “Pharmacodynamics and pharmacokinetics of higher-dose, double- bolus eptifibatide in percutaneous coronary intervention.” Circulation. 2001 Jul 24;104(4):406-11.

Kandzari DE, Behar VS, Skektch MH Jr., Keriakes DJ, Shimshak T, Broderick T, Young J, Runyon JP, Safian RD, Kern M, Colombo A. “Extensive thrombus prior to elective percutaneous coronary intervention.” J Invasive Cardiol. 2001 Jul:13(7):538-42.

Keriakes DJ, Young JJ, Runyon JP, Shimshak TM. “Ticlopidine monotherapy following coronary stent deployment: penny wise and pound foolish.” J Invasive Cardiol. 2001 Jun;13(16):437-8.

Dippel EJ, Keriakes DJ, Tramuta DA, Broderick TM, Shimshak TM, Roth EM, Hattemer CR, Runyon, JP, Whang DD, Schneider JR, Abbottsmith, CW. “Coronary perforation during percutaneous coronary intervention in the era of abciximab platelet glycoprotein IIB/IIIa blockade: an algorithm for percutaneous management.” Catheter Cardiovasc Interv. 2001 Mar;52(3):279-86.

Runyon, JP, Snavely DD. “Rapid dissolution of intracoronary thrombus with eptifibatide therapy in a patient with post-infarction angina.” J Invasiv Cardiol. 2000 Dec; 12 Suppl D4D-7D.

Keriakes DJ, Obenchain RL, Barber BL, Smith A, McDonald M, Broderick TM, Runyon JP, Shimshak TM, Schneider JF, Hattemer CR, Roth EM, Whang DD, Cocks D, Abbottsmith CW. “Abciximab provides cost-effective survival advantage in high-volume interventional practice.” Am Heart J. 2000 Oct;140(4):603-10.

Keriakes, DJ, Runyon JP, Broderick TM, Shimshak TM. “IIb’s are not IIb’s.” Am J Cardiol. 2000 Apr 27;85(8A):23C-31C.

Runyon, JP. “Facilitated percutaneous coronary intervention: validating the open artery hypothesis.” J Invasive Cardiol. 2000 Mar; 12 Suppl B:22B-25B.

Keriakes DJ, Broderick TM, Roth EM, Whang D, Shimshak T, Runyon JP, Hattemer C, Schneider J, Lacock P, Muyeller M, Abbottsmith, CW. “Time course, magnitude, and consistency of platelet inhibition by abciximab, tirofiban, or eptifibatide in patients with unstable angina pectoris undergoing percutaneous coronary intervention.” Am J Cardiol. 1999 Aug 15;84(4):391-5.

Keriakes DJ, Kleiman NS, Ferguson JJ, Masud AR, Broderick TM, Abbottsmith CW, Runyon JP, Anderson LC, Anders RJ, Drelling RJ, Hantsbarger GL, Bryzinski B, Rtopoll EJ. “Pharmacodynamic efficacy, clinical safety, and outcomes after prolonged platelet glycoprotein IIB/IIIa receptor blockade with oral Xemilofiban: Results of a multicenter, placebo-controlled, randomized trial.” Circulation. 1998 Sept. 29:98(13):1268-78.

Keriakes DJ, Kleiman N., Ferguson JJ, Runyon JP, Roderick TM, Higby NA, Martin LH, Hantsbarger G, McDonald S, Anders RJ. “Sustained platelet glycoprotein IIb/IIIa blockade with oral Xemilofibal in 111 patients after coronary stent deployment.” Circulation. 1997 Aug 19:96(4): 1117-21.

Keriakes DJ, Kleiman N, Ferguson JJ, Runyon JP, et al: Sustained Platelet Glycoprotein IlB/IIIa Blockade with Oral Xemilofiban in 170 Patients After Coronary Stent Deployment. Circulation. 1997: Aug; 96(4):1117.

Kereiakes DJ, Essell JH, Abbottsmith CW, Broderick TM, Runyon JP: Abciximab-Associated Profound Thrombocytopenia: Therapy with Immunoglobulin and Platelet Transfusion. American Journal of Cardiology. 1996: Nov; 78:1161-1163.

Runyon, JP, et al. “Abciximab-associated profound thrombocytopenia: therapy with immunoglobulin and platelet transfusion.” Am J Cardiol. 1996 Nov. 15;78(10):1161-3.

Keriakes DJ, Runyon JP, Kleiman NS, Higby NA, Anderson LC, Hantsbarger G, McDonald S, Anders RJ. “Differential dose-response to oral Xemilofiban after antecedent intravenous Aciximab administration for complex coronary intervention.” Circulation. 1996 Sept. 1;94(5)906-10.

Kereiakes DJ, Runyon JP, et al. “Differential Dose-Response to Oral Xemilofiban After Antecedent Intravenous Abciximab.” Circulation. 1996: Sept 1; 94(5):906-910.

Gibler WB, Runyon JP, Levy RC, Sayre MR, Kacich, R, Hattemer CR, Hamilton C, Gerlach JW, Walsh RA. “A rapid diagnostic and treatment center in the emergency department for patients with chest pain.” Ann Emerg Med. 1995 Jan;25(1):1-8.

Gibler WB, Sayre MR, Levy RC, Runyon JP, Kacich R., Hamilton C, Walsh RA. “Serial 12-lead electrocardiographic monitoring in patients presenting to the emergency department with chest pain.” J Electrocardiol. 1993:26 (Suppl):238-43.

Gibler WB, WalshRA, LevyRC, RunyonJP.“Rapid Diagnostic and Treatment Center in the Emergency Department for Patients with Chest Pain.” Submitted, American Heart Association, 65th Scientific Sessions, November, 1992.

Runyon JP, Gerson MC: “Noninvasive Test Selection in the Coronary Care Unit,” in Cardiac Nuclear Medicine, 2nd ed., edited by Myron C. Gerson. McGraw Hill, New York, 1991, pp. 337-386.

Links – John Paul Runyon

The following are links to John Paul Runyon’s other websites, blogs and social media:

WEBSITES

JohnPaulRunyon.com

JohnPaulRunyon.org

JohnPaulRunyon.net

John-Paul-Runyon.com

JohnPaulRunyonInfo.com

BLOGS

WordPress

Tumblr

Weebly