Photography by Brian Goddard Suns forward Channing Frye was diagnosed with an enlarged heart last September. He hopes to return to the court next season.

A PHOENIX magazine editor scours the Valley for answers to his heart disease, consulting cardiovascular comrades like Suns player Channing Frye and local doctors.


Well, this is it,” the surgeon says, with an encouraging smile. “As you can see, it’s pretty compact. Nothing so terrible.”

Admittedly, the smooth, teardrop-shaped device in his hand – slightly larger than a Zippo lighter, and the same silvery color – is hardly terrifying. And it is relatively small. By smartphone standards, for example, it would be record-breakingly compact.
 
But since the man holding it wants to cut open my chest and implant the device under my collarbone, along with three barbed electrical wires that will slither into my heart and nest there like prop pythons from an Indiana Jones flick, the sight of this gizmo chills me to the bone. It might as well be a suitcase bomb.
 
“Will people be able to see it?” I ask, vainly considering the cosmetic consequences.
 
By way of response, the physician takes my hand and guides it to the area just above his left shirt pocket. The large bump underneath feels solid and unyielding, as if someone taped a pager to his chest.

Ah, so, I think. The heart-club president is also a client.

“When you have your shirt on, no one will know it’s there,” he says. When you have your shirt on. But when you don’t, it’ll look like a gerbil crawled under your skin and died on your chest.

At 41 years old, I’m not too old to care how an Implanted Cardioverter Defibrillator (ICD) will look when I casually take my shirt off at the beach. Still, as a proud recipient of hereditary heart disease, I’m precisely the kind of person who needs one – specifically, the kind of person who might kick over and die at any second.

For me and people like me – a not-so-hearty group that includes professional athletes, amateur athletes, students, moms, dads and folks from every walk of life, including, as I will later learn, at least one standup comedian – the ICD is an effective stop-gap measure against cardiac disaster. It’s also crudely invasive and fraught with risk. And it looks bad. So, despite this doctor’s rather kind display of commiseration, I leave his office with little or no intention of opting for ICD surgery. Besides, there are whispers of a new, less invasive ICD in the Valley, and before giving up one’s active, non-chest-gerbil-impeded lifestyle, isn’t it prudent to check out every option?

Illustration Courtesy of Boston Scientific Shocker: Artist's illustration of the new, less invasive S-ICD, which delivers a life-saving shock through the breastplate.

My condition is called hypertrophic cardiomyopathy (HCM), informally known as “enlarged heart,” and even more informally known as “that thing that causes sudden death in young athletes,” most famously Loyola Marymount basketball star Hank Gathers and NBA All-Star Reggie Lewis. Dozens of young Arizonans have died from the disease, including former Mountain Pointe High football player Anthony Bates, whose mother, Sharon, subsequently launched a foundation in his name dedicated to raising awareness of HCM.
 
For many HCM sufferers – which is to say, the unluckiest HCM sufferers – the first and only symptom is cardiac arrest and death, often in the midst of strenuous activity. More fortunate patients experience non-lethal symptoms like chest pain, light-headedness and heart murmurs. That’s what I have – heart murmurs. Almost non-stop for 15 years.
 
I remember clearly the moment of my first murmur – or, at least, the first one I felt. It was on a drive to Sedona. The desert landscape was just pleasantly rolling by when my heart stopped – if only for a beat. Two quick beats later the organ was back in rhythm, a brief disruption to be sure, but long enough that it inspired a rising lump of alarm in my throat. Later, I would tell friends that it was like being tapped on the shoulder by mortality itself. Nothing too dramatic or painful. Just a tap. A reminder.

Hey, bro. Remember me?

Around the same time, I also had my first abnormal electrocardiogram (EKG) – the standard frontline test for abnormal heart rhythms. Referred to a cardiologist, I took comfort in the initial diagnosis: athlete’s heart, a condition marked by slight cardiac over-muscling, due to vigorous exercise. “You have nothing to worry about,” the cardiologist told me, with a recommendation to take magnesium supplements for the heart murmurs.
 
I was in my late 20s at this point, and none too eager to entertain the thought of a serious heart ailment. So I let the diagnosis ride, even as the tappings became more intense and frequent, and even as members of my family started getting diagnosed with HCM. Finally, years later, a second visit to the cardiologist revealed a dramatic thickening of the heart’s central structure, the septum, and its main chamber, the left ventricle, both definitive pathologies of HCM. The thickening is caused by an overabundance of muscle cells, laid on top of each other willy-nilly in a way that disrupts the heart’s natural electrical flow, a phenomenon known as myocardial disarray.

There are varying degrees of severity in the estimated 600,000 Americans afflicted with HCM; mine was deemed on the severe side of moderate. By no means a death sentence, but critical enough that my risk-averse cardiologist recommended the ICD.

Best-case scenario: You go through life never knowing you have the disease, and die old and happy. Worst-case scenario: The hardened, over-muscled ventricle can’t eject blood properly and one day slips into a spastic electrical state called a ventricular fibrillation. Like a car engine sucking in air, it seizes, and you go into cardiac arrest. If that happens, you better hope there’s somebody nearby with paramedic-style shock paddles, or that you’ve been equipped with one of those Zippo-sized ICDs, which perform essentially the same function.
 
Your chances of surviving cardiac arrest without immediate electrical defibrillation? About the same as hitting 00 in roulette. Which is to say: not terrific.

Dr. Thomas Mattioni of Arizona Arrhythmia Consultants, currently the only electrocardiology clinic in Arizona offering the S-ICD.

After receiving my HCM diagnosis, I did the only natural thing: I went on the Internet and found out which celebrities had it, too. Unfortunately, most of them are not with us anymore. Names like Gathers and Lewis and strongman Jesse Marunde. Ex post facto, it was revealed that late actor Corey Haim had HCM; though heart failure and pneumonia figured prominently in the official autopsy, years of vigorous post-stardom substance abuse also played a role in his demise, one would imagine.

Last summer, when Phoenix Suns power forward Channing Frye announced he was taking a sabbatical due to an enlarged heart, I felt a pang of empathy, and interest. Like many Phoenix-area basketball fans, I admire the way Frye handles himself, from his deadeye perimeter shooting – so rare in a player of his 6-foot-11 stature – to his upbeat court presence and smart locker room sound bites. I imagined us bro-ing out over HCM war stories.
 
As it turns out, Frye wasn’t diagnosed with hypertrophic cardiomyopathy, but its Bizarro World sibling: dilated cardiomyopathy (DCM). DCM affects the same part of the heart as HCM but in the completely opposite way – instead of becoming overmuscled and cramped, the stricken ventricle expands and loses tensile strength like a piece of worn elastic. Ultimately, the chamber simply becomes too vast and capacious for the compromised muscle to handle.
 
Though they take opposite routes, DCM and HCM arrive at the same ultimate destination: ventricular fibrillation and cardiac arrest, in the worst cases.

Curious about Frye’s prognosis – and interested in his course of treatment – I meet him on the Suns practice court one weekday morning after team shootaround. The first thing I learn is that DCM, unlike HCM, is not necessarily hereditary or genetic. In clinical terms, it’s most often idiopathic – meaning physicians don’t know what causes it.

“It’s definitely not genetic with me because I didn’t have it last year or any year,” Frye says reasonably. “They think I probably got sick and a combination of being sick and traveling and overexertion of my body caused [the heart ailment].”

Frye suspected that something was wrong with his health shortly after the conclusion of the strike-shortened 2011-2012 NBA season. Despite twice-daily workouts over the summer, he was getting winded on stairways and was constantly tired. He tried chalking up the fatigue to the eight weeks of down-time that followed his shoulder surgery in April, but a routine pre-season physical in September settled the matter: He had cardiomyopathy, possibly caused by the combination of a draining strike season in which NBA teams played an impacted schedule; stress caused by his infant daughter’s double cataract surgery; and a theoretical virus that may have taken advantage of Frye’s compromised immune system.


For the rest of PHOENIX magazine’s 'Broken Hearts Club', check back soon, find us at newsstands Valleywide or call 480-664-3960.  Subscribe today so you don’t miss another issue!