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The Hospitalist. 2005 September;2005(09):

Not all Troponin Elevations Are Myocardial Infarctions

Jeremais A, Gibson CM. Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded. Ann Intern Med. 2005;142:786-791.

Troponins are regulatory proteins that control the calcium-mediated interaction of actin and myosin during muscle contraction. All muscle tissue contains troponins, but cardiac troponin T and I have amino acid sequences that are different from skeletal and smooth muscle troponins, allowing them to be detectable by monoclonal antibody-based assays.

In the event of reversible or irreversible cell damage—or possibly even from transiently increased cell membrane permeability—cardiac troponins are released from myocytes into circulation. This characteristic provides a sensitive test for detecting myocardial injury and damage; however, this test is not specific for acute coronary syndromes. And any disorder that causes myocyte damage may cause an elevated troponin.

The 2002 American College of Cardiology/American Heart Association practice guidelines for unstable angina and non-ST-segment elevation myocardial infarction acknowledge that the myocardial necrosis signified by troponin elevation may not necessarily be caused by atherosclerotic coronary artery disease. Such nonthrombotic troponin elevation can be caused by four basic mechanisms, as discussed by Dr. Jeremias and Dr. Gibson.

  1. Demand ischemia refers to a mismatch between myocardial oxygen demand and supply in the absence of flow-limiting epicardial stenosis. Conditions such as sepsis or septic shock and the systemic inflammatory response syndrome, hypotension or hypovolemia, tachyarrhythmias, and left ventricular hypertrophy can all cause release of cardiac troponin.
  2. Myocardial ischemia in the absence of fixed obstructive coronary disease can be caused by coronary vasospasm, acute stroke or intracranial hemorrhage, and ingestion of sympathomimetics.
  3. Direct myocardial damage can be seen in cardiac contusion, direct current cardioversion, cardiac infiltrative disorders such as amyloidosis, certain chemotherapy agents, myocarditis, pericarditis, and cardiac transplantation.
  4. Myocardial strain occurs when volume and pressure overload of the left and/or right ventricle cause excessive wall tension. Congestive heat failure, acute pulmonary embolism, and chronic pulmonary hypertension can lead to myocardial strain and troponin elevation.

Another condition that can lead to persistently elevated cardiac troponins is end-stage renal disease. This elevation may be due to small areas of clinically silent myocardial necrosis, an increased left ventricular mass, or possibly from impaired renal troponin excretion. Although troponins are believed to be cleared by the reticuloendothelial system, recent evidence shows that troponin T is fragmented into molecules that are small enough to be renally excreted.

In summary, elevated troponin can be found in many clinical settings and is associated with impaired short- and long-term survival. TH

Classic Literature

The HATEFUL Patient

Every physician has groaned internally when seeing a certain patient’s name on his list, going out of her way to avoid a particular family, or getting hopelessly engaged and increasingly enraged in a battle over a “lost” narcotic prescription. There are certain patients with whom a doctor-patient relationship feels more like a contest than a partnership. These interactions make a physician’s daily practice difficult, and they may wreak havoc among the staff on an inpatient ward. These patients grow ever more intolerable to their caregivers, who often harbor a wish to simply make them disappear.

In his landmark 1978 article “Taking Care of the Hateful Patient,” (NEJM, 298:883-887) James Groves, MD, discussed the characteristics of these difficult patients and the sometimes difficult emotions they generate in their caregivers. He described four different groups of patients, using an illustrative case for each, and discussed the ways in which these patients’ often maddening behavior serves to mitigate their profound dependency.

Dependent clingers are those patients whose neediness is overt, who seem to regard the physician as a sow with teats to spare. Dr. Groves suggested early, firm limit-setting with these patients to prevent the formation and later shattering of the patient’s illusion of the physician as inexhaustible.

There are certain patients with whom a doctor-patient relationship feels more like a contest than a partnership.

Dependency lies at the heart of an entitled demander’s behavior as well, but their fear of abandonment is expressed as hostility and arrogance rather than overt neediness. Affirming to the patient that you share in their quest for the good (but not perfect) medical care to which they are entitled allows patient and physician to rally around a common goal.

This strategy backfires with manipulative help-rejecters, who seem almost pleased to report to their physician each time they fail a new treatment attempt. Overtly expressing some doubt that the treatment will completely cure all the patient’s difficulties and providing regular follow up are recommended for this group. These strategies relieve the patient of the unconscious anxiety that he may be abandoned by his physician should his symptoms abate.

Self-destructive deniers make the physician feel powerless as they persist in behavior that undermines all efforts to improve their health. With these patients, viewing their behavior as a terminal illness and managing symptoms and exacerbations accordingly allows the physician to focus on caring for the patient without unrealistic expectations of cure on the one hand and judgmental indifference on the other.

After discussing each of these groups, Dr. Groves concluded the article by suggesting that perhaps the greatest challenge physicians face in caring for these difficult patients is the temptation to disown the negative feelings they engender. He wrote that this effort not only strains the doctor’s limits, but also wastes valuable clinical data unmasked by these feelings—data that could inform clinical care. For decades prior to Dr. Groves’ article, psychoanalysts had reflected on what Freud termed “countertransference,” or the physician’s internal emotional reaction to a patient.

In his article “Hate in the Counter-Transference,” D.W. Winnicott, MD, suggested that rather than accepting the guilt that these feelings typically engender in a caregiver, negative countertransference reactions should be regarded by the physician as valuable information in understanding the patient’s psychic world. By training and by disposition, however, most physicians considered (and continue to consider) these emotions inappropriate. They seemingly negate the sympathy, kindness, and commitment to the patient’s well-being that should be central to a physician’s vocation. Conventional wisdom held that denying the feelings was the only proper response, and if that proved impossible, transferring the patient to a willing colleague was usually recommended. In contrast, Dr. Groves freed the physician to use these feelings to improve patient care.

Now a classic and oft-cited work, “Taking Care of the Hateful Patient” distills a wealth of analytic insight into a structure and language comprehensible to the busy generalist. By explaining the reactions each group of patients induces in their physicians, Dr. Groves provides useful tools to understand a particular patient’s psychology. Suggestions for strategic approaches to each category of patient are easy to understand and to adapt to one’s own practice. He explains how judicious limit-setting can be as valuable for the patient as it is for the doctor. Perhaps most helpful is his description of the needs of these patients that lie beneath their “hateful” exterior. Armed with this understanding, a physician can reclaim the empathy that is often so elusive with these patients.—Sandra Rackley MD, Kemuel Philbrick, MD