Allan S. Jaffe

Severe depression is associated with markedly reduced heart rate variability in patients with stable coronary heart disease

OBJECTIVEnThe purpose of this study was to investigate the relationship between depression and heart rate variability in cardiac patients.nnnMETHODSnHeart rate variability was measured during 24-hour ambulatory electrocardiographic (ECG) monitoring in 40 medically stable out-patients with documented coronary heart disease meeting current diagnostic criteria for major depression, and 32 nondepressed, but otherwise comparable, patients. Patients discontinued beta-blockers and antidepressant medications at the time of study. Depressed patients were classified as mildly (n = 21) or moderately-to-severely depressed (n = 19) on the basis of Beck Depression Inventory scores.nnnRESULTSnThere were no significant differences among the groups in age, gender, blood pressure, history of myocardial infarction, diabetes, or smoking. Heart rates were higher and nearly all indices of heart rate variability were significantly reduced in the moderately-to-severely versus the nondepressed group. Heart rates were also higher and mean values for heart rate variability lower in the mildly depressed group compared with the nondepressed group, but these differences did not attain statistical significance.nnnCONCLUSIONnThe association of moderate to severe depression with reduced heart rate variability in patients with stable coronary heart disease may reflect altered cardiac autonomic modulation and may explain their increased risk for mortality.

Major depression, heart rate, and plasma norepinephrine in patients with coronary heart disease

BACKGROUNDnAlthough it is now well established that psychiatric depression is associated with adverse outcomes in patients with coronary heart disease (CHD), the mechanism underlying this association is unclear. Elevated heart rate (HR) and plasma norepinephrine (NE), possibly reflecting altered autonomic nervous system activity, have been documented in medically well depressed psychiatric patients, and this pattern is associated with increased risk for cardiac events in patients with CHD. The purpose of this study was to determine whether autonomic nervous system activity is altered in depressed CHD patients.nnnMETHODSnHR, plasma NE, and blood pressure (BP) were measured in 50 depressed and 39 medically comparable nondepressed CHD patients at rest and during orthostatic challenge.nnnRESULTSnResting HR (p = .005), and the change from resting HR at 2, 5, and 10 min after standing (p = .02, .004, and .02, respectively), were significantly higher in the depressed than in the nondepressed patients. There were no differences between the groups in NE or in BP at rest, or in standing minus resting change scores at any time during orthostatic challenge (p < .05).nnnCONCLUSIONSnDepression is associated with altered autonomic activity in patients with CHD, as reflected by elevated resting HR and an exaggerated HR response to orthostatic challenge. Previously reported differences in NE levels between depressed and nondepressed patients were not replicated.

Cardiac troponin I in pediatrics: Normal values and potential use in the assessment of cardiac injury

OBJECTIVEnTo establish normal values and determine the impact of congenital or acquired heart disease on serum cardiac troponin I (cTnI).nnnMETHODSnConcentrations of cTnI were measured in two groups of children. Group A represented ambulatory pediatric patients with no apparent cardiac disease (n = 120) and patients in stable condition with known congenital or acquired cardiac abnormalities (n = 96); group B was composed of patients admitted to intensive care units with normal echocardiograms (n = 16), with abnormal echocardiograms (n = 36), and those with blunt chest trauma who were thought to have cardiac contusions (n = 7).nnnRESULTSnThe cTnI concentrations were generally less than 2.0 ng/ml in group A and frequently below the level of detection for the assay (1.5 ng/ml). There was no statistical difference between the two outpatient subgroups (p = 0.66). Nine intensive care patients had cTnI values greater than 2.0 ng/ml. Six of these patients, all with abnormal echocardiograms, had values less than 7.7 ng/ml. All improved and had subsequent normal cTnI concentrations. None of the three remaining patients (two with systemic illness (trauma and sepsis) and one with severe pulmonary hypertension), all with values greater than 8.0 ng/ml, survived. Three of the four patients with high likelihood of cardiac contusion had cTnI concentrations greater than 2.0 ng/ml (including one patient who died).nnnCONCLUSIONSnCardiac troponin-I values are generally not elevated in children with stable cardiac disease or general pediatric conditions. In the context of severe acute illness, significant elevation of cTnI may be an indicator of poor outcome. Elevation of cTnI may also have diagnostic value in cases when cardiac contusion is suspected.

Transient Right but Not Left Ventricular Dysfunction After Strenuous Exercise at High Altitude

OBJECTIVESnWe sought to evaluate whether prolonged exercise in ultramarathon runners results in left ventricular (LV) damage.nnnBACKGROUNDnStrenuous exercise has been reported to cause LV damage.nnnMETHODSnFourteen runners who completed an ultramarathon at high altitude underwent echocardiography, finger-tip oximetry and blood measurements of cardiac troponin I (cTnI) and creatine kinase, MB fraction (CK-MB) levels before, immediately after and 1 day after the race.nnnRESULTSnAt baseline, the echocardiograms showed normal LV and right ventricular (RV) size and function in all subjects, as well as mild tricuspid regurgitation in nine subjects, with normal estimated pulmonary artery systolic pressure (mean 28 mm Hg). At baseline, all oxymetric readings and CK-MB measurements were normal, and cTnI was undetectable. Immediately after the race, the echocardiograms showed the expected augmentation of global and segmental LV function in all subjects. Although the RV was normal in nine subjects, five developed marked RV dilation and hypokinesia, paradoxic septal motion, pulmonary hypertension and wheezing. CK-MB values were elevated in all subjects. In all but one subject cTnI was undetectable. In that subject there was a small elevation in cTnI accompanied by severe RV dysfunction and pulmonary hypertension. At the 1-day follow-up study, the echocardiographic measurements had normalized in all subjects.nnnCONCLUSIONSnIn trained athletes, strenuous exercise at high altitude did not result in LV damage. However, wheezing, reversible pulmonary hypertension and RV dysfunction occurred in a third of those completing the race. The incidence and pathogenesis of these findings remain to be determined.

Cardiac Troponin I Levels Are Normal or Minimally Elevated After Transthoracic Cardioversion

OBJECTIVESnThe present study was designed to assess the impact of direct current shocks on cardiac troponin I (cTnI), which has greater sensitivity and specificity than creatine kinase (CK) for the diagnosis of myocardial injury.nnnBACKGROUNDnTransthoracic direct current shocks can cause myocardial injury. They also cause elevations of total CK and CK-MB fraction (CK-MB).nnnMETHODSnWe obtained measurements of cTnI total CK and CK-MB before and after elective cardioversions in 38 patients. Blood samples were drawn before and 8, 16, 24 and 48 h after cardioversion. Shock energy, current, impedance and number of shocks delivered were tabulated.nnnRESULTSnPatients received a mean (+/-SD) of 2.1 +/- 1.2 shocks with a median cumulative energy of 300 J (range 50 to 1,580). Three patients had minimal elevations (1.5, 1.2 and 0.8 ng/ml, normal < or = 0.6 ng/ml) of cTnI. Two of these patients had impaired left ventricular contractility by echocardiography. Thirty-five of the 38 patients had no elevations of cTnI. Sixty-two percent of patients had an increase in CK after cardioversion, but CK-MB was elevated to an abnormal level of 12.7 ng/ml (normal < 6.7) in only one patient after cardioversion.nnnCONCLUSIONSnCardiac troponin I levels are either normal or minimally elevated after elective direct current cardioversion, suggesting that subtle myocardial injury can be caused by direct current transthoracic shocks. However, substantial elevations of cTnI after cardioversion suggest the presence of myocardial injury from causes unrelated to the direct current shocks administered for cardioversion.

Can treating depression reduce mortality after an acute myocardial infarction

Major depression affects about one in five patients in the weeks after an acute myocardial infarction and is associated with an increased risk of cardiac morbidity and mortality. Consequently, there is considerable interest in the question of whether treating depression will improve medical prognosis in these patients. Safe, effective treatments for depression are available, but unless they also improve the underlying pathophysiological or behavioral mechanisms that contribute to cardiac morbidity and mortality, they may not have beneficial effects on prognosis. Altered cardiac autonomic tone is one of the leading candidate mechanisms. Unfortunately, a review of the available research reveals that cardiac autonomic tone often fails to normalize in patients treated for depression, and the research suggests that currently available treatments for depression will not necessarily improve cardiac event-free survival in patients who have had an acute myocardial infarction. Until there is convincing evidence that treatment can reduce the risk of cardiac morbidity and mortality, the principal reason to treat depression should continue to be to improve the quality of life of the patient who has had an acute myocardial infarction. Key words: depression, coronary heart disease, mortality.

Adherence to a prophylactic medication regimen in patients with symptomatic versus asymptomatic ischemic heart disease

Although angina pectoris is the most common symptom of coronary artery disease, some patients do not experience angina during ischemic episodes. The effects of asymptomatic (silent) heart disease on patient self-management have rarely been studied. Studies of other patient populations with asymptomatic illnesses indicate that patients with silent myocardial ischemia might adhere less well to a prophylactic medication regimen than would those with symptomatic ischemia. Depression, a state associated with poor adherence to medical regimens is more common among patients with symptomatic ischemia. For prevention of thromboembolic events, 37 patients with documented ischemic heart disease who denied having anginal symptoms and 28 patients who reported almost daily symptoms were given a 3-week supply of low-dose aspirin packaged in an unobtrusive electronic adherence monitor. All other medications were provided in standard pill bottles. The symptomatic patients removed their prescribed aspirin on 62.4% of the days; the patients with silent ischemia took their medication on 77.3% of the days. Possible explanations for these results, their clinical implications, and directions for future research are discussed.

2001 — A biomarker odyssey

It is a time of transition in the area of biomarkers. Confusion is rampant, progress immense and the challenges invigorating. Better diagnosis is possible if we progress in a rational way and avoid the chaos so often characteristic of transitions by relying on the science of the discipline to keep us on track.

Use of serum markers of myocardial injury for the early diagnosis of acute myocardial infarction

Summary Newer methods for diagnosing acute myocardial infarction are available. Each strategy and marker has its pros and cons. The additive value of these markers diagnostically and particularly in providing beneficial alternative treatment options over the use of the ECG alone requires further definition.

Traumatic intracardiac thrombus

A 36-year-old male was seen in the emergency room after being hit by a car while riding a snowmobile; on admission, he was hemodynamically stable. He had multiple fractures with a right pneumothorax requiring a chest tube. Because of possible myocardial injury, he was evaluated with a transesophageal echocardiogram that revealed an abnormal motion of the right ventricle and a left atrial septal thrombus (Fig. 1, arrow) through a patent foramen ovale (Fig. 2, arrow). Serial transthoracic echocardiograms showed persistence of the thrombus. The patient was placed on a heparin drip and was subsequently started on Coumadin (DuPont Pharmaceuticals, Wilmington, DE). Nine days postinjury, a cardiac MRI did not demonstrate the thrombus, and it had decreased significantly by echocardiographic evaluation. The patient did well with the anticoagulation. LA, left atrium; RA, right atrium; Ao, aorta; LV, left ventricle; RV, right ventricle.