The heart never takes a holiday. Over the course of a lifetime, this amazing pump can expect to beat more than 3 billion times. No disruptions, no breaks, no rest days. And anything that stands in the way of a beating heart represents a potentially fatal hurdle. We’re all going to die of something and 1 in 6 of us are going to die directly from heart attacks. This isn’t necessarily a bad thing, because if we cut down the number of cardiac deaths, then by definition we have to increase the number of people dying from sepsis, cancer, stroke, emphysema, and accidents. As morbid as this sounds, eliminating cardiac disease is a misplaced goal if it means dying a slow painful death from cancer, or the inexorable wasting away of Alzheimer’s. Given the option of a quick and relatively painless death at age 95 from a heart attack, I believe most of us would sign the dotted line in a literal heartbeat. And here’s the good news; the age-adjusted mortality for heart disease has decreased by 50% over the last 30 years, with half that decline attributed to risk factor modification (smoking, diabetes, hypertension, and hyperlipidemia), and the other half due to improvements in treatment. Sudden cardiac death still happens in the form of massive non-survivable heart attacks and sudden malignant rhythm disturbances (ventricular fibrillation), but know that, if you get to the hospital in time, your chance of survival is quite good.

Heart disease constitutes a spectrum of conditions ranging from rhythm disturbances to heart failure to arterial blockages. It is the last that leads to angina, which occurs when the heart muscle is deprived of oxygen (ischemia). In practice, angina occurs in 3 situations; from chronic blockages related to atherosclerotic plaque, from acute blockages due to clots, and occasionally from coronary artery spasm even in the absence of pre-existing disease (e.g. cocaine). Angina is reversible. Restoring blood flow relieves the pain. A heart attack, on the other hand, occurs when oxygen deprivation progresses to the point of muscle death. Dead heart doesn’t conduct electricity normally, and this provides the basis through which EKGs are used to diagnose heart attacks. Dead muscle cannot be restored but the damage can be mitigated with prompt intervention.

 

 

Now you might think that the heart would always be well-supplied with oxygen. After all, it’s full of blood! But as it turns out, the heart isn’t able to extract this life-sustaining molecule from the blood swirling through its chambers. It’s only after leaving the heart that blood finds its way into the muscle via the coronary arteries (so named because, once-upon-a-time, somebody thought the arteries atop the heart resembled the staves of a king’s crown). Heart attacks occur when blockages arise in these vessels. Symptoms include—but are not limited to—chest pain, shortness of breath, sweating, lightheadedness, and nausea. Sometimes there is just an overwhelming sense of fatigue without any pain at all. When pain does occur, it is typically below the breastbone and described as a “heaviness” or “pressure” (“like an elephant sitting on my chest”), but may also be sharp, dull, achy, or burning. Heart pain may not even occur in the chest. The general rule of thumb is that pain anywhere from “the nose to the naval” might be cardiac in origin. It’s truly an unfortunate happenstance that the brain is unable to precisely localize the source of internal organ pain. “Heartburn” shouldn’t be called heartburn at all; it should be called stomach burn, but the quality of heartburn may exactly mimic a heart attack and vice-versa.

For acute chest pain, there is a lot to be done. Call 9-1-1 from any metropolitan area in the nation and you will likely be met by an ambulance within minutes. Paramedics will check your blood pressure, pulse, respiratory rate, and oxygen saturation. You will be placed on a cardiac monitor while an IV is inserted. You will be given aspirin to chew. You may receive nitroglycerin under your tongue or morphine through the IV. Most ambulances are now equipped with EKG telemetry machines that allow medics to send a 12-lead tracing to the nearest hospital. For those with training, recognizing an acute heart attack on an EKG (known as a “STEMI” for ST Elevation Myocardial Infarction) is as easy as reading the word “cat.” If you’re lucky enough to have your heart attack during routine working hours then you will likely be met, not only by an emergency physician and a bevy of well-trained nurses, but also by an interventional cardiologist. After placement of an ID bracelet, a blood draw, a confirmatory EKG, and perhaps a chest x-ray, you will be whisked toot-sweet to the cardiac catheterization lab.

Once a catheter has been snaked up into the coronary circulation, dye injected into the arteries followed by a series of x-rays can accurately locate occlusions that may then be opened with PTCA (percutaneous transluminal coronary angioplasty). This procedure involves placing a deflated balloon-tipped catheter into the site of the blockage and then inflating the balloon to flatten out the vessel wall. This is almost always followed by the placement of an expandable metal stent across the site to maintain patency. Sometimes the blockage is in a site not amenable to PTCA, or there are multiple large blockages, in which case you will likely be referred for CABG (coronary artery bypass grafting). These procedures have reduced the in-hospital mortality from heart attacks, which used to be on the order of 25-30%, down to just 5%. So why am I skeptical?

As it turns out, fewer than half of the annual 500,000 PCI procedures performed in the US are done to treat heart attacks. The majority are performed for stable coronary artery disease despite evidence that stents placed for this indication are of little or no benefit. As opposed to someone having an acute heart attack, let’s assume you’re a 50-yeard old man who felt especially fatigued after cutting the grass last weekend. On thinking back, you realize that you’ve been feeling increasingly tired of late and have been short-winded when negotiating the 2 flights of steps to your office. Let’s assume further that you have hypertension and high cholesterol both controlled with medication, and that your father had his first heart attack at age 51. Not wanting to ignore these symptoms—after all, the cemetery is full of people who thought to themselves, just a little indigestion is all—you make an appointment with your primary care physician. He sees you in the office where your EKG has some mild changes, but “nothing to worry about.” You’re scheduled for a stress test, and although you feel okay during the test, the results are equivocal.

Calcium Score          Presence of Coronary Artery Disease

0                                              No Evidence of Disease

1-10                                          Minimal Evidence of Disease

11-100                                      Mild Evidence of Disease

101-400                                   Moderate Evidence of Disease

over 400                                  Extensive Evidence of Disease

Your doctor refers you to a cardiologist. After tweaking your medications, she schedules you for a coronary artery calcium score. The test employs a CT scanner to gauge the total amount of calcium within your coronary arteries, where the score (from 0 to greater than 400) is a surrogate marker for atherosclerotic plaque. While higher scores correlate to significant plaque build-up and subsequent adverse cardiac events, the test is unable to determine whether any single vessel is blocked to dangerous levels. If the score is zero (which occurs in roughly a quarter of low risk symptomatic patients) then you’re in the clear. Unfortunately, while the test is highly sensitive (almost everybody with significant blockages has a positive score), the coronary artery calcium score is not specific for the disease in question (up to 60% of people without significant blockages have positive scores). Your test comes back at 100, an equivocal number that implies a mild to moderate risk of an important blockage. Many cardiologists, at this point, would recommend proceeding directly to a cardiac catheterization, but sensing your reticence she orders a CCTA (coronary CT angiogram) instead. This test employs sophisticated computerized technology to reconstruct images of the coronary arteries, providing essentially the same information as PCI but without the catheter. The test is more sensitive and specific than a coronary calcium score, but also employs considerably more radiation, increasing a middle-aged adult’s lifetime risk of a fatal cancer by roughly 1 in 2,000. (Sorry, no free ride.) Also, if a significant blockage is present, a cardiac catheterization is still required to treat it. Let’s assume that this study, too, is abnormal, demonstrating a 50% blockage in one of the major coronary arteries, along with lesser blockages in several others. This is not surprising but rather the expected result for a middle-aged man with risk factors for heart disease. Fortunately, blockages of 50% rarely cause heart attacks and the cardiologist recommends continued medical therapy and adds an aspirin to your meds that already include 2 blood pressure pills and a statin.

 

 

You feel lucky but are still worried about that blockage. You fall into a funk and start noticing a steady-state, low-level anxiety creeping into your world. You vow to change your diet and begin a regular walking program. For a few weeks all is well, but then life intervenes and you start slacking. By the time football season is in full swing, you are back to full couch-potato mode. Three months later a bout of chest pain while raking leaves sets you off in a panic to the ER. Nothing has changed on your EKG and your heart muscle enzyme tests (Troponin) come back normal. Since you’ve already undergone a stress test, coronary artery calcium score, and coronary CT angiogram there are no other tests to perform in the ER, and 8 hours later you are released. The cause of your chest pain is unclear. Was it indigestion? Was it your heart? Was it simple muscle strain or anxiety? The ER doctor doesn’t know (which pisses you off), but then writes for a bottle of tiny nitroglycerin tablets and tells you to place one under your tongue every 5 minutes and call 9-1-1 if you have additional chest pain. This scares the shit out of you, and convinces you that a catheterization is necessary. A week later you have the procedure and everything goes well. Your cardiologist places a stent across the blockage. Plavix is added to your medications, but not before she reads you the riot act about how you can never miss a dose without running the risk of the stent clotting off. Physically you feel fine, but emotionally you’re not so hot. Your family doctor adds an antidepressant and a sleeping pill, bringing the number of daily medicines to 6, along with 2 as-needed drugs. Everybody is trying to help. You feel like these people saved your life. The bill for all this testing comes out to more than $50,000. Did you get your money’s worth?

Despite the fact that this scenario plays out hundreds of thousands of times a year in the US, the answer is “No.” As opposed to acute heart attacks where stent placement can be life-saving, stents for stable coronary artery disease don’t help. And we’ve known this for a long time. The first study showing the lack of benefit appeared in 2007, in an issue of the New England Journal of Medicine, where nearly 2,300 patients were randomized to either optimal medical treatment versus medical treatment plus catheterization/stent (PCI). Over a median follow up of 4.6 years there were only trivial differences in death, heart attack, stroke, and hospitalization rates between the groups, all of which favored medical management over catheterization. (It turns out that the procedure itself caused a few heart attacks). The only benefit was a reported decrease in angina in the catheterization group, but at an estimated cost of $150,000 per patient who got relief. Most patients didn’t benefit at all. Subsequent studies yielded similar results, and in what should have been the final nail in the coffin, a meta-analysis appeared in 2012 combining the results of 8 prior trials of more than 7,200 patients again showing no benefit to PCI over standard medical therapy. In this larger data base, the intervention didn’t even relieve angina.

Once again, evidence defies logic. It makes sense that opening a blockage should prevent heart attacks and relieve angina but it doesn’t. Why? Well, here is the interesting part; while blockages of 75% or more are likely to result in angina symptoms, they are also more organized and less likely to rupture. They’ve been there longer and are more stable than smaller plaques. Heart attacks typically occur when a plaque ruptures and acute clot forms around the site of injury resulting in a sudden total, or near-total, occlusion of the vessel. Dissolving the clot and opening this sort of blockage with a stent is life-saving. For large stable plaques, however, stenting doesn’t help. Despite recommendations by the American Heart Association, more than half of all cardiac catheterizations to evaluate stable coronary artery disease patients are conducted prior to initiating optimal medical therapy. Eliminating even a third of these procedures would save the system between $6-8 billion annually.

So why do we keep doing them? Money, of course. Cardiac catheterizations are huge revenue generators, not just for cardiologists but also for hospitals. It’s a hard sell to tell a hospital to stop allowing a procedure that is the only thing keeping it in the black. It’s also a hard sell to cardiologists. I am totally empathetic with their plight. When confronted by a patient with coronary artery disease and ongoing symptoms, saying, “Doc, you gotta do something,” shrugging your shoulders won’t cut it. Clearly, something has to be done, but shouldn’t that something be based on evidence? You know, like diet and exercise. Stay out of the cath lab. Keep running, cycling, and skating. Eat well. Breathe …

 

References:

1. Earl Ford et al., “Explaining the Decrease in U.S. Deaths from Coronary Artery Disease,” NEJM 2007; 356: 2388-98.
2. “Heart Attack—In Depth Report,” New York Times; nytimes.com/health/guides/disease/heart-attack/print.html.
3. Paul Chan et al., “Appropriateness of Percutaneous Coronary Intervention,” JAMA 2011; 306 (1): 53-61.
4. Mark Pletcher et al, “What Does My Patient’s Coronary Artery Calcium Score Mean? Combining Information from the Coronary Artery Calcium Score with Information from Conventional Risk Factors to Estimate Coronary Heart Disease Risk,” BMC Med 2004; 2: 31
5. William Boden et al., “Optimal Medical Therapy with or without PCI for Stable Coronary Disease,” NEJM 2007; 356 (15): 3503-16.
6. William Weintraub et al., “Cost-Effectiveness of Percutaneous Coronary Intervention in Optimally Treated Coronary Patients,” Circ Cardiovasc Qual Outcomes 2008; 1: 12-20.
7. Kathleen Stergiopoulos and David Brown, “Initial Coronary Stent Implantation with Medical Therapy vs Medical Therapy Alone for Stable Coronary Artery Disease: Meta-Analysis of Randomized Controlled Trial,” Arch Int Med 2012; 172 (4): 312-19.
8. William Boden, “Mounting Evidence for Lack of PCI Benefit in Stable Ischemic Heart Disease,” Arch Int Med 2012; 172 (4): 319-21.
9. Nicholas Bakalar, “No Extra Benefits Are Seen in Stents for Coronary Artery Disease,” NY Times; Feb 27, 2012: nytimes.com/2012/02/28/helath/stents-show-no-extra-benefits-for-coronary-artery-disease.html.
10. Stephan Fihn at al., “2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients with Stable Ischemic Herat Disease: Executive Summary,” J Am College Card 2012; 60 (24): 2654-2603.