Pat Risser (Patrick)

154 Ronald Ave.

Ashland, OH  44805

(503) 655-2530 – home

(419) 908-9335 – cell


Emergency Contact:

Patricia Sandoval (significant other)


Heart Problem


I visited a cardiologist on Monday, January 7, 2008 and he said my heart has suffered substantial and significant deterioration.  He recommended a defibrillator implant ASAP.


His lack of bedside manner and the callous way in which he interacted with me and Trish really put us off.  It felt like he had delivered an emotional gut punch and issued me a death sentence.


We decided that the best thing was to gather more information and be retested and obtain a second (and perhaps a third or fourth) opinion.  I am in no pain or discomfort.  The only symptom is feeling tired and short of breath.  Overall, my spirits are good and I am pretty much doing everything I've ever done.


I had to see my primary care doc to get a referral to another cardiologist for a second opinion.  I saw the cardiologist on Tuesday, January 22, 2008.  He confirmed the diagnosis and recommendation.  I saw the cardiac electrophysiologist who will do the surgery on Thursday, January 24, 2008.


The cardiologists said my heart is bad ("ejection fraction 15") to the point where I was high risk of sudden cardiac death.  That's those folks you hear about who are eating dinner and suddenly slump over dead or the guy who is watching TV and just keels over dead or the woman who goes to sleep and never wakes up.


A bunch of years ago, sudden cardiac death episodes (ventricular fibrillation) would kill 97%.  Once in a while, paramedics would show up, zap the person with the paddles and restart their heart.  Only 3% survived and those were the candidates that got defibrillator implants.  Eventually, heart docs got a clue and started to think about what the risk factors were and started putting defibrillators in those who might have an episode.


I'm one of those who might have an episode.  Of those who get defibrillators, a year later, 2 will not have needed it.  But, one will come in and shake the docs hand and say thanks for saving my life.  There's no way to predict which one of the three I will be.  I might live the rest of my life and never have an episode.  On the other hand, if an episode should occur my chances of survival are very high with the implant.


I went into the hospital and had the surgery done on Monday, January 28, 2008 at MedCentral Hospital in Mansfield.  I went in the morning, had surgery in the afternoon and was discharged on Tuesday around noon.  I went home to rest and recover.  It'll take a few days/weeks to heal but I'll have the comfort of the "insurance" of knowing I'll likely survive if I have a future episode of ventricular fibrillation.


I'm still a bit sore (a three-inch wound to put in a device the size of a small deck of cards or a large pocket watch) from being sliced open like cutting open a pork chop to stuff it.  I can't drive for ten days and I'm not supposed to lift my arm too high but I am healing slowly.  Actually, I think I'm probably healing quickly under the circumstances.  Modern medicine is amazing.  I tried to ask them to take me back in next week for the rest of the bionics (both legs and my pitching arm) but they didn't think my Medicare would cover it.


Thanks for caring. 




Current Heart History (most recent first)


February 5, 2008

Follow-up with Jon Benson, PA-C for removal of bandage

Mid-Ohio Heart Clinic

680 Park Avenue West

Mansfield, OH 44906

(419) 524-8151


January 29, 2008

Discharged from MedCentral Hospital in Mansfield, Ohio hospital around noon

MedCentral Hospital

335 Glessner Ave.

Mansfield, OH 44903



January 28, 2008

Monday, 11:00 a.m.

Went into MedCentral Hospital in Mansfield, Ohio for surgical implant of

Medtronic Virtuoso VR Defibrillator

Surgeon was: Dr. Jeffery P. Courson, D.O.

Mid-Ohio Heart Clinic

680 Park Avenue West

Mansfield, OH 44906

(419) 524-8151

MedCentral Hospital

335 Glessner Ave.

Mansfield, OH 44903



January 24, 2008

Thursday, 9:15 a.m.

See Cardiac Electrophysiologist

Dr. Jeffery P. Courson, D.O.

Mid-Ohio Heart Clinic

680 Park Avenue West

Mansfield, OH 44906

(419) 524-8151


January 22, 2008

Tuesday, 10:00 a.m.

See Cardiologist

Dr. Andrew Fahmy

Samaritan Medical Clinic Building

350 Hillcrest Drive

Ashland, Ohio 44805

Main Office:

680 Park Avenue West

Mansfield, OH 44906

(419) 524-8151

Confirmed diagnosis and strongly recommended defibrillator implant and made referral to Cardiac Electrophysiologist, Jeffery P. Courson, D.O. in the Mansfield office


January 18, 2008

Friday, 2:10 p.m.

See Primary Care Physician

Dr. Stephen Torski

2111 Claremont Ave.

Ashland, OH 44805

(419) 281-5575

Receeived referral for 2nd opinion to cardiologist Dr. Andrew Fahmy


January 7, 2008

Monday, 3:30 p.m.

See Cardiologist

Dr. Bruce Fleishman, MD, FACC

At Samaritan Hospital Ashland, OH

(419) 289-0491 x-3501

Said, "heart has substantially and significantly deteriorated" and recommended a Defibrillator implant


December 21, 2007

Friday, 11:30 a.m.

Samaritan hospital for blood work and Echocardiogram


December 20, 2007

Thursday, 2:30 p.m.

See Primary Care Physician

Dr. Stephen Torski

2111 Claremont Ave.

Ashland, OH 44805

(419) 281-5575

Ordered blood work, Echocardiogram and referral to cardiologist Bruce Fleishman



Medical/Family History


Medical History:

      Born in Ashland, Ohio September 24, 1952 at Samaritan Hospital

      Tonsils out 1954

      First three heart attacks, Feb. 14, Mar. 7, Dec. 23, 1988 (Dr. Joseph Connelly, Denver, Colorado)

      Fourth heart attack October 13, 1994 (cardiologist: Dr. Jacque Chahin, Concord, California)

      Fifth heart attack January 27, 1997 (cardiologist: Dr. Mark Hattenhauer, Tualatin, Oregon) with stent implant;

      Then follow-up with Dr. William Davies, 19260 SW 65th Ave., Pacific Heart Associates, Tualatin, OR 97062-5712. Phone, (503) 692-0405

      Appendix out July 22, 2006 (Samaritan Hospital) (while there, heart had atrial tachycardia and diagnosis of ischemic cardiomyopathy)



      Serious major needle phobia

      No major broken bones

      No known allergies

      General health good

      Started smoking age 7

      Quit smoking December 2001 (age 49)


Family History:

      Maternal grandfather died of heart attack age 60

      Other grandparents died old age


      Mother generally healthy (born 10-30-32; age 75)

      Father (Eldred Risser) died in auto accident August 15, 1954

      Maternal Aunt deceased around 1996 from apparent stroke

      Maternal Uncle deceased September 30, 1999 suicide

      Maternal Uncle with "heart problems" age 67


      Brother Mike (one year younger; born 09-25-53) had stroke age 25, stent implants for heart issues in his 40's and carotid cleared

      Brother Rich (2 ½ year younger; born 04-30-55) claims he takes nitro, is schizoaffective, is alcoholic


      Daughter Bridget born 1973 (healthy)

      Daughter Heather born 1975 (healthy)

      Son John born 1979 (healthy)



      Moved to Denver, Colorado 1960

      Moved to Mayfield Hts., Ohio 1968

      Graduated Mayfield HS 1970

      Married 1972, moved to Colorado

      Moved to Cleveland 1973

      Moved to Colorado 1978

      Graduated Colorado College with BA, Philosophy 1983

      Attended Denver University Law School 1983-1985

      Moved to California 1990

      Moved to Oregon 1996

      Moved to Ashland, Ohio October 2005



Daily Pills: (No Known Allergies)



Lotensin (Benazepril Hcl – 10 mg.)

Coreg (25 mg.)

Lipitor (10 mg.)

Furosemide (Lasix – 20 mg.)

Folic Acid (400 mcg.)

Multi-Vitamin OneSource for adults 50+

B-12 (500 mcg.)

Glucosamine Chondroitin Complex (1500 mg. and 1200 mg.)



Lotensin (Benazepril Hcl – 10 mg.)

Coreg (12.5 mg.)

Allopurinol (150 mg.)

Aspirin (325 mg.)

Niacin (time-released 500 mg.)

Vitamin C (500 mg.)

Vitamin E (400 I.U.)

Glucosamine Chondroitin Complex (1500 mg. and 1200 mg.)



Background for Heart info

This is my primary diagnosis:

Ischemic cardiomyopathy


Ischemic cardiomyopathy is a weakness in the muscle of the heart due to inadequate oxygen delivery to the myocardium with coronary artery disease being the most common cause. Anemia and sleep apnea are relatively common conditions that can contribute to ischemic myocardium and hyperthyroidism can cause a 'relative' ischemia secondary to high output heart failure. Individuals with ischemic cardiomyopathy typically have a history of myocardial infarction (heart attack), although longstanding ischemia can cause enough damage to the myocardium to precipitate a clinically significant cardiomyopathy even in the absence of myocardial infarction. In a typical presentation, the area of the heart affected by a myocardial infarction will initially become necrotic as it dies, and will then be replaced by scar tissue (fibrosis). This fibrotic tissue is akinetic; it is no longer muscle and cannot contribute to the heart's function as a pump. If the akinetic region of the heart is substantial enough, the affected side of the heart (i.e. the left or right side) will go into failure, and this failure is the functional result of an ischemic cardiomyopathy.


Cardiomyopathy, which literally means "heart muscle disease", is the deterioration of the function of the myocardium (i.e., the actual heart muscle) for any reason. People with cardiomyopathy are often at risk of arrhythmia or sudden cardiac death or both.  This is the reason why my cardiologist has recommended:


Implantable Cardioverter-Defibrillator (ICD)


Also known as Automatic Internal Cardiac Defibrillator (AICD). These devices are implants, similar to pacemakers (and many can also perform the pacemaking function). They constantly monitor the patient's heart rhythm, and automatically administer shocks for various life threatening arrhythmias, according to the device's programming. Many modern devices can distinguish between ventricular fibrillation, ventricular tachycardia, and more benign arrhythmias like supraventricular tachycardia and atrial fibrillation. Some devices may attempt overdrive pacing prior to synchronised cardioversion. When the life threatening arrhythmia is ventricular fibrillation, the device is programmed to proceed immediately to an unsynchronized shock.


There are cases where the patient's ICD may fire constantly or inappropriately This is considered a medical emergency, as it depletes the device's battery life, causes significant discomfort and anxiety to the patient, and in some cases may actually trigger life threatening arrhythmias. Some emergency medical services personnel are now equipped with a ring magnet to place over the device, which effectively disables the shock function of the device while still allowing the pacemaker to function (if the device is so equipped). If the device is shocking frequently, but appropriately, EMS personnel may administer sedation.


An implantable cardioverter-defibrillator (ICD),



also known as an automated implantable cardioverter-defibrillator (AICD), is a small battery-powered electrical impulse generator which is implanted in patients who are at risk of sudden cardiac death due to ventricular fibrillation. The device is programmed to detect cardiac arrhythmia and correct it by delivering a jolt of electricity. In current variants, the ability to revert ventricular fibrillation has been extended to include both atrial and ventricular arrhythmias as well as the ability to perform biventricular pacing in patients with congestive heart failure or bradycardia.


The process of implantation of an ICD is similar to implantation of a pacemaker. Similar to pacemakers, these devices typically include electrode wire/s which pass through a vein to the right chambers of the heart, usually being lodged in the apex of the right ventricle. The difference is that pacemakers are more often temporary and generally designed to consistently correct bradycardia, while AICDs are often permanent safeguards against sudden abnormalities.


ICDs constantly monitor the rate and rhythm of the heart and can deliver therapies, by way of an electrical shock, when the electrical manifestions of the heart activity exceeds the preset number. More modern devices can distinguish between ventricular fibrillation and ventricular tachycardia (VT), and may try to pace the heart faster than its intrinsic rate in the case of VT, to try to break the tachycardia before it progresses to ventricular fibrillation. This is known as fast-pacing, overdrive pacing, or anti-tachycardia pacing (ATP). ATP is only effective if the underlying rhythm is ventricular tachycardia, and is never effective if the rhythm is ventricular fibrillation.


Many modern ICDs use a combination of various methods to determine if a fast rhythm is normal, ventricular tachycardia, or ventricular fibrillation.


Rate discrimination evaluates the rate of the lower chambers of the heart (the ventricles) and compares it to the rate in the upper chambers of the heart (the atria). If the rate in the atria is faster than or equal to the rate in the ventricles, then the rhythm is most likely not ventricular in origin, and is usually more benign. If this is the case, the ICD does not provide any therapy.


Rhythm discrimination will see how regular a ventricular tachycardia is. Generally, ventricular tachycardia is regular. If the rhythm is irregular, it is usually due to conduction of an irregular rhythm that originates in the atria, such as atrial fibrillation.


Morphology discrimination checks the morphology of every ventricular beat and compares it to what the ICD believes is a normally conducted ventricular impulse for the patient. This normal ventricular impulse is often an average of a multiple of beats of the patient taken in the recent past.


In July 2006 when I had my appendix out, my heart showed Atrial fibrillation.


Atrial fibrillation (AF or afib) is a cardiac arrhythmia (abnormal heart rhythm) that involves the two upper chambers (atria) of the heart. It is defined as being irregularly irregular, and can often be identified as such when taking a pulse. Atrial fibrillation is the most common arrhythmia; risk increases with age, with 8% of people over 80 having AF. In atrial fibrillation, the electrical impulses that are normally generated by the sinoatrial node are replaced by disorganized activity in the atria, leading to irregular conduction of impulses to the ventricles that generate the heartbeat. The result is an irregular heartbeat. This may be continuous (persistent or permanent AF) or alternating between periods of a normal heart rhythm (paroxysmal AF). The natural tendency of atrial fibrillation is to become a chronic condition. Chronic AF leads to an increased risk of death.


Atrial fibrillation is often asymptomatic, and is not in itself generally life-threatening, but may result in palpitations, fainting, chest pain, or congestive heart failure. Patients with atrial fibrillation are at significantly increased chance of stroke (about 2 to 7 times the regular population), and AF is a leading cause of stroke.


Atrial fibrillation may be treated with medications which either slow the heart rate or revert the heart rhythm back to normal. Synchronized electrical cardioversion may also be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent recurrence of atrial fibrillation in certain individuals. People with AF are often given anticoagulants such as warfarin to protect them from stroke.


In cardiovascular physiology, ejection fraction (Ef) is the fraction of blood pumped out of a ventricle with each heart beat.  Normal is between 55 and 70.  My ejection fraction is 15.


Damage to the muscle of the heart (myocardium), such as that sustained during myocardial infarction or in cardiomyopathy, impairs the heart's ability to eject blood and therefore reduces ejection fraction. This reduction in the ejection fraction can manifest itself clinically as heart failure. The ejection fraction is one of the most important predictors of prognosis; those with significantly reduced ejection fractions typically have a poorer prognoses.