Anterior Myocardial Ischemia Research Articles

Myocardial perfusion defects after radiation therapy and anthracycline chemotherapy for left breast cancer: a possible marker of microvascular damage. Three cases and review of the literature.

Radiation therapy to the thorax may induce early and late cardiac adverse effects if large parts of the heart have been included in the irradiation field and particularly if anthracycline-containing chemotherapy is concomitantly administered. We describe 3 cases of cardiotoxicity in patients with left breast cancer treated with anthracycline-containing chemotherapy and left thoracic radiotherapy. In 2 cases we observed asymptomatic electrocardiographic abnormalities of ventricular repolarization mimicking anterior myocardial ischemia and SPECT reversible myocardial perfusion defects. In 1 case we observed echocardiographic abnormalities of left ventricular wall motion and reversible myocardial perfusion abnormalities. We recommend close cardiac monitoring of patients treated with anthracycline chemotherapy and left thoracic radiotherapy to better understand the clinical impact of these abnormalities.

Dose-Dependent Cardioprotection of Moderate (32°C) Versus Mild (35°C) Therapeutic Hypothermia in Porcine Acute Myocardial Infarction

ObjectivesThe study investigated whether a dose response exists between myocardial salvage and the depth of therapeutic hypothermia. BackgroundCardiac protection from mild hypothermia during acute myocardial infarction (AMI) has yielded equivocal clinical trial results. Rapid, deeper hypothermia may improve myocardial salvage. MethodsSwine (n = 24) undergoing AMI were assigned to 3 reperfusion groups: normothermia (38°C) and mild (35°C) and moderate (32°C) hypothermia. One-hour anterior myocardial ischemia was followed by rapid endovascular cooling to target reperfusion temperature. Cooling began 30 min before reperfusion. Target temperature was reached before reperfusion and was maintained for 60 min. Infarct size (IS) was assessed on day 6 using cardiac magnetic resonance, triphenyl tetrazolium chloride, and histopathology. ResultsTriphenyl tetrazolium chloride area at risk (AAR) was equivalent in all groups (p = 0.2), but 32°C exhibited 77% and 91% reductions in IS size per AAR compared with 35°C and 38°C, respectively (AAR: 38°C, 45 ± 12%; 35°C, 17 ± 10%; 32°C, 4 ± 4%; p < 0.001) and comparable reductions per LV mass (LV mass: 38°C, 14 ± 5%; 35°C, 5 ± 3%; 32°C 1 ± 1%; p < 0.001). Importantly, 32°C showed a lower IS AAR (p = 0.013) and increased immunohistochemical granulation tissue versus 35°C, indicating higher tissue salvage. Delayed-enhancement cardiac magnetic resonance IS LV also showed marked reduction at 32°C (38°C: 10 ± 4%, p < 0.001; 35°C: 8 ± 3%; 32°C: 3 ± 2%, p < 0.001). Cardiac output on day 6 was only preserved at 32°C (reduction in cardiac output: 38°C, –29 ± 19%, p = 0.041; 35°C: –17 ± 33%; 32°C: –1 ± 28%, p = 0.041). Using linear regression, the predicted IS reduction was 6.7% (AAR) and 2.1% (LV) per every 1°C reperfusion temperature decrease. ConclusionsModerate (32°C) therapeutic hypothermia demonstrated superior and near-complete cardioprotection compared with 35°C and control, warranting further investigation into clinical applications.

Abstract 10868: Prognostic Value of Fragmented QRS Localization for Myocardial Ischemia and Left Ventricular Dyssynchrony: Analysis Using Semiconductor Single Photon Emission Computed Tomography

Introduction: Fragmented QRS (fQRS) in 12-lead electrocardiography is reported to be a predictor of cardiac prognosis in ischemic heart disease. In contrast, certain studies have reported that fQRS is associated with cardiac resynchronization therapy response. However, few studies have evaluated the diagnostic performance of local fQRS using semiconductor single photon emission computed tomography (SPECT). Hypothesis: fQRS is a powerful indicator of anterior myocardial ischemia and left ventricular (LV) dyssynchrony. Methods: A total of 740 consecutive sinus rhythm patients with various cardiac diseases underwent SPECT with adenosine stress. The local fQRS was classified into I/aVL/V5-6 (lateral), II/III/aVF (inferior), and V1-4 (anterior). Cases with wide QRS (&gt;120ms), obvious right bundle branch block, and where fQRS existed in multi-classes were excluded. A 17-segment model of myocardial perfusion SPECT was divided into 3 areas: anterior, inferior, and lateral. Each summed score at rest (SRS), under stress (SSS), and the difference (SDS) was calculated. Results: fQRS was present in 82 cases (lateral, 13; anterior, 15; inferior, 54) and analysis of variance showed that anterior SSS was significantly higher in anterior fQRS cases (p=0.012). Histogram bandwidth of LV contraction onset - a known dyssynchrony parameter - was significantly higher in lateral fQRS cases (p135 degrees and SD&gt;43 degree, lateral fQRS had a high OR (7.91) with significant 95%CI (2.32-27.0) for indicating the condition. Conclusions: fQRS in anterior leads is a significant indicator of anterior wall ischemia; and fQRS in lateral leads is a significant indicator of LV dyssynchrony.

Sequential moderate coronary artery fistula and moderate coronary artery stenosis causing ischemia demonstrated by fractional flow reserve and relieved following percutaneous coronary intervention

Coronary artery fistulae are rare anomalous connections arising from the coronary circulation. We report a case of anterior wall myocardial ischemia caused by the combination of sequential coronary-to-pulmonary artery fistula and moderate (50-60%) stenosis of the left anterior descending coronary artery. Ischemia was demonstrated by myocardial stress perfusion imaging as well as fractional flow reserve. Percutaneous coronary intervention of the lesion resulted in resolution of ischemia.

Abstract 18300: Myocardial Ischemia Induces Telomerase Activity in the Mouse Heart

Introduction: The incidence of cardiovascular disease rises with age. Ischemia and oxidative stress-induced DNA damage and telomere erosion may accelerate cardiac senescence. The enzyme telomerase has been shown to protect cardiovascular cells from mitochondrial oxidative stress independent of telomere elongation. We examined whether myocardial ischemia impacts on telomere biology and cellular aging in the infarcted mouse heart. Methods and results: C57Bl/6 mice (10 weeks old, n=6-8 per group) were subjected to anterior myocardial ischemia induced by proximal ligation of the left anterior descendant coronary artery or sham operation. Cardiac MRI was used to verify infarct localization and measure LV function, showing that ejection fraction was reduced in MI mice (47±5% vs. 68±3% in sham, p&lt;0.01). Sham and MI mice were compared 3 days, 7 days, or 4 weeks after LAD ligation and myocardial infarct zone (IZ) and remote zone (RZ) were analyzed. Telomerase activity as measured by TRAP assays was elevated in the infarct zone 3 days after LAD ligation (187±9% vs. sham mice, p&lt;0.01), but not in the remote zone (113±35%). Seven days after myocardial infarction, telomerase was up-regulated both, in the infarct zone (177±31%) and the remote zone (154±26%). This effect was even more pronounced 4 weeks after LAD ligation (IZ: 271±14%; RZ 223±28%). In concert with telomerase activation, telomere repeat binding factor (TRF) 2 protein expression was up-regulated in the infarct zone after three days (337±25%) and in both areas after 7 days (IZ: 431±48%; RZ: 380±31%) and less strongly after 4 weeks (IZ: 170±23%; RZ: 141±27%). In parallel to telomerase activity and TRF2 expression, the apoptosis and senescence markers p53 (189±11%), Chk2 (167±32%), bax/bcl2-ratio (278±27%) and p16 (518±42%) were up-regulated in the myocardium of MI mice after 4 weeks (all shown values p&lt;0.05 vs. myocardial tissue of sham-operated mice). Conclusion: Myocardial telomerase and telomere-associated factors are up-regulated in a time- and region-specific manner in the infarcted mouse heart in concert with apoptosis and cell-cycle regulators. This regulatory process may be of relevance for myocardial survival, inflammation, and remodelling after ischemia.

Severe coronary spasm occasionally detected by coronary computed tomography

Coronary spasm not only plays an important role in coronary spastic angina but also in ischae- mic heart diseases in general, and the incidence is quite high among Japanese. Coronary spasm can be reliably detected by an intracoronary injection of acetylcholine (ACh) during cardiac catheterization, but not by coronary computed tomography (CT) because coronary spasm is transient, occurs mostly between midnight and the early morning and rarely during the daytime. When a patient undergoes coronary CT at our institution, we routinely administer sublingual nitroglycerine to maximally dilate cor- onary arteries. Thus, we were totally unaware of the possibility of coronary spasm occurring during coronary CT, which did occur in a 41-year-old man and is described herein. Cardiac catheterization as an examination for chest pain at rest did not reveal any significant changes in coronary arteriograms. The patient's symptoms were mild and atypical for angina pec- toris, and only nitroglycerin was prescribed. Six months later, electrocardiography in a regular outpatient clinic revealed abnormal QS mor- phology in leads V1-V4 indicating severe anterior myocardial ischaemia without specific symptoms. A second CAG was a provocative test for coronary spasm using ACh which revealed coronary spasm. Organic stenosis was also identified at Segment 6 of the left anterior descending artery (LAD). Per- cutaneous coronary intervention (PCI) using balloon angioplasty was performed. Thereafter, the patient was prescribed with medi- cation for angina pectoris. Five years later, the patient developed chest pain during exertion and was examined by coronary dual-source CT (DSCT). The results showed almost total occlusion of Segment 1 of the right coronary artery (RCA) (Panels A and B). A third CAG was planned considering PCI for the most recently identified region. No significant stenosis was evident in the LAD, but collateral arteries to the RCA via the septal branches indicated total or subtotal chronic occlusion of the RCA (Panel C). We injected nitroglycerine into the LAD to arrange PCI and then infused the RCA with contrast dye. Surprisingly, only 25% stenosis of Segment 1 was evident (Panel D) and immediate angiography of the LAD showed that the collateral arteries had dis- appeared, indicating that a severe and spontaneous coronary spasm had occurred immediately before PCI and that the total occlusion identified by DSCT was due to coronary spasm. Calcium channel blockers were then administered, which effectively treated his con- dition for now. Silent spasm frequently occurs among patients with coronary spasm, and this should be considered when analysing coronary CT images. This report is the first description of severe coronary spasm being detected by coronary CT. Panels (A and B) Arrows show significant coronary stenosis in Segment 1 of the right coronary artery detected by coronary com- puted tomography.

Left anterior descending coronary artery myocardial bridging by multislice computed tomography: Correlation with clinical findings

Objective To assess the relationship between left anterior descending (LAD) coronary artery myocardial bridging detected by 64-slice computed tomography (CT) and clinical findings. Methods 221 consecutive patients were examined with coronary 64-slice CT angiography. 21 patients with coronary stenosis >50% were excluded. The length, depth, and luminal narrowing of LAD myocardial bridges during systole and diastole were measured. CT findings were compared with the treadmill ECG-stress test, and clinical symptoms. Results Myocardial bridges of the LAD were found in 23% of patients (51/221) (length, 14.9 ± 6.5 mm; depth, 2.6 ± 1.6 mm). A significant difference was noted between the LAD luminal diameter before the intramyocardial course and intramyocardially, for both diastole and systole ( p < 0.001); with a higher diameter reduction of 27% for end-systole compared to end-diastole with 15% ( p = 0.006). Systolic LAD intramyocardial luminal narrowing >50% was found in 3/25 (8%). 30/51 (59%) of bridges were “deep” (>2 mm myocardial depth), 21/51 (41%) were “superficial”. The prevalence of a positive ECG-stress tests for the anterior myocardial region was significantly higher in patients with LAD myocardial bridges (34/50; 68%) compared to those without (28/144; 19.4%) ( p < 0.001). There was no difference between “superficial” and “deep” LAD myocardial bridges in regard to a positive treadmill ECG-stress test. Typical angina was rare with 6%. Conclusion LAD myocardial bridges are common findings and can possibly explain a positive exercise ECG-stress test for anterior myocardial ischemia. Intramyocardial LAD segments show mild-to-moderate luminal narrowing at rest, which is higher during end-systolic phase.

Myocardial Perfusion Defects after Radiation Therapy and Anthracycline Chemotherapy for Left Breast Cancer: A Possible Marker of Microvascular Damage. Three Cases and Review of the Literature

Radiation therapy to the thorax may induce early and late cardiac adverse effects if large parts of the heart have been included in the irradiation field and particularly if anthracycline-containing chemotherapy is concomitantly administered. We describe 3 cases of cardiotoxicity in patients with left breast cancer treated with anthracycline-containing chemotherapy and left thoracic radiotherapy. In 2 cases we observed asymptomatic electrocardiographic abnormalities of ventricular repolarization mimicking anterior myocardial ischemia and SPECT reversible myocardial perfusion defects. In 1 case we observed echocardiographic abnormalities of left ventricular wall motion and reversible myocardial perfusion abnormalities. We recommend close cardiac monitoring of patients treated with anthracycline chemotherapy and left thoracic radiotherapy to better understand the clinical impact of these abnormalities.

P38 Mitogen-Activated Protein Kinase Inhibition Decreases TNFalpha Secretion and Protects Against Left Ventricular Remodeling in Rats with Myocardial Ischemia

The purpose of this study was to test our hypothesis that p38 mitogen-activated protein kinase (p38 MAPK) inhibitor SB203580 may favorably affect tumor necrosis factor alpha (TNFalpha) secretion and left ventricular (LV) remodeling after myocardial ischemia (MI). The left anterior descending coronary artery (LAD) was ligated to produce anterior MI in 40 rats that were randomly divided into two groups: p38i group (n = 24) and MIR group (MI rat models, n = 24). A sham operation group without LAD ligation (Sham, n = 16) was also studied. SB203580 (2 mg/kg) and saline was injected i.p. once every 3 days in the first two groups, respectively. One and six weeks after MI, cardiac function, myocardial fibrosis, the cardiac expressions of phosphorylated p38 MAPK (p-p38 MAPK), TNFalpha, alpha smooth muscle actin (alphaSMA) and collagen I, the ultramicrostructure of the myocardium were examined by echocardiography, histological staining, western blot, immunohistochemical staining, transmission electron microscope (TEM), respectively. Treatments with SB203580 suppressed myocardial fibrosis and LV remodeling, as well as attenuated the expressions of p-p38-MAPK, TNFalpha, alphaSMA and collagen I as compared with the MIR. In conclusion, SB203850 has an effect of inhibiting inflammation-induced fibrosis, which leads to attenuation of LV remodeling.

Interaction between left ventricular wall motion and intraventricular flow propagation in acute and chronic ischemia

Myocardial ischemia has been associated with left ventricular (LV) postsystolic shortening. The combination of tissue Doppler imaging and high frame-rate acquisition of two-dimensional color flow makes it possible to study the interaction between LV wall motion and intraventricular flow propagation. The aim of this study was to examine in a clinical model the impact that acute myocardial ischemia and prior myocardial infarct might have on LV flow patterns and to explain the underlying mechanisms from the tissue Doppler data. LV flow propagation and tissue velocities during early diastole were studied in 18 healthy individuals, 17 patients with prior anterior myocardial infarct, and 16 patients before and during percutaneous coronary intervention (PCI) of the left anterior descending artery. Normal individuals had intraventricular flow propagation toward the apex during isovolumic relaxation. During this early diastolic time phase, myocardial velocities measured at mid- and apical septal segment were directed away from the apex. Before PCI, patients without myocardial infarction had similar findings as in normal individuals. In contrast, each patient with either prior myocardial infarction or PCI-induced acute ischemia had flow propagation opposite to normal individuals, and tissue velocities reversed toward the apex during early diastole. Reversal of early diastolic LV flow propagation in acute and chronic anterior myocardial ischemia reflects postsystolic shortening in the dyskinetic apical and septal myocardial segments.

EXPRESSION OF MHC AND MCT1 IN CARDIAC MYOCYTES AFTER EXERCISE TRAINING IN MYOCARDIAL INFARCTED RATS

Previous studies show that cardiac metabolism becomes more dependent on glucose and lactate as an important cellular respiratory substrate in the failing heart. However, the effect of exercise training on monocarboxylate transporter (MCT 1) and lactate utilizatio in the failing heart remains unclear. PURPOSE The purpose of this study was to investigate the effects of mild exercise training on cardiac myosin heavy chain (MHC) isoforms, which is related to the energy efficiency in muscle contraction, and MCT 1 after surgically induced anterior myocardial ischemia (MI) in a rat model. METHODS Male Wistar rats (250□} 10 g) were randomly assigned to four groups: i) sedentary sham (SS, n=5); ii) sedentary MI (SMI, n=7); iii) exercise sham (ES, n=6); iv) exercise MI (EMI, n=8). MI was produced by occlusion of the left coronary artery for 30 minutes. Exercise training was accomplished using a running protocol in which animals ran on a motor treadmill at 10m/min for 60min/day, 5 d/wk for 6 weeks. The wall of the left ventricle was dissected and divided into anterior wall (AW, ischemic region) and posterior wall (PW). Citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (HAD) activities were measured by biochemical assays. The separation of MHC was performed using SDS-PAGE. Western blotting was used to detect the MCT1 expression. RESULTS Acute MI impaired CS and HAD activities in the AW (p < 0.001) but not in the PW. The relative amount of MHC- fÀ in both AW and PW were significantly increased in acute MI animals. However, exercise training resulted in a significant reduction of MHC-fÀ expression in both AW and PW (p < 0.01). The expression of MCT1 in both AW and PW was not affected by acute MI (8% increase in SMI compared to SS, p > 0.05), whereas exercise training significantly increased the expression of MCT 1 in ES by 65% vs. SS and in EMI by 34% vs. SMI (p < 0.05) in PW. CONCLUSION These findings suggest that exercise training enhances the MCT1 and MHC-f¿ expression in cardiac myocytes in rats with acute myocardial infarction.

Effectiveness of adjunctive stent implantation following directional coronary atherectomy for treatment of left anterior descending ostial stenosis

The aim of this study was to evaluate the acute and long-term angiographic and clinical results of optimal plaque debulking by means of directional coronary atherectomy (DCA) followed by stent implantation for treatment of left anterior descending (LAD) ostial stenosis. Eighty consecutive patients (66 men; aged 57 ± 10 years) with angina pectoris, documented anterior myocardial ischemia, and de novo LAD ostial stenosis prospectively underwent DCA and stent deployment. They were evaluated angiographically after 6 months and clinically for up to 30 ± 29 months. The primary success rate was 98%. The in-hospital complications were 1 death due to in-stent subacute thrombosis 7 days after the procedure, 1 non–Q-wave myocardial infarction, and 1 retrograde left main artery dissection. The angiographic binary restenosis rate was 14.5%, and the loss index was 0.38 ± 0.35. The target lesion revascularization (TLR) rates at 6, 12, and 24 months were 6.0%, 14.5%, and 16.3%, respectively, and the combined event rates (death, nonfatal myocardial infarction, TLR) at the same times were 8.7%, 17.5%, and 21.2%, respectively. These results indicate that the combined approach of DCA and stent implantation is feasible and safe in patients with LAD ostial lesions, has a high success rate, a low incidence of restenosis, and a good long-term outcome.

Outpatient Chemotherapy: Hypersensitivity and Anaphylaxis

Outpatient Chemotherapy: Hypersensitivity and Anaphylaxis

Anomalous origin of the left coronary artery from the pulmonary artery with large anterior myocardial infarction and ischemia: successful tunnel repair and concomitant heterotopic heart transplantation as biological bridge to recovery

Anomalous origin of the left coronary artery from the pulmonary artery with large anterior myocardial infarction and ischemia: successful tunnel repair and concomitant heterotopic heart transplantation as biological bridge to recovery

Reflection of Epicardial U-Wave Changes in Surface Inferior Electrocardiograms During Inferoposterior or Anterior Wall Myocardial Ischemia

The surface inferior electrocardiogram (ECG) has limited value for detecting frequently occurring epicardial U-wave changes over the ischemic inferoposterior wall. Reciprocal U-wave changes could occur in this ECG during anterior wall myocardial ischemia.

How epicardial U-wave changes are reflected in body surface precordial electrocardiograms in anterior or inferoposterior myocardial ischaemia during coronary angioplasty.

To examine the epicardial U-wave changes recorded in intracoronary electrocardiograms (ECGs) during anterior or inferoposterior myocardial ischaemia and the corresponding changes in precordial ECGs recorded from the body surface in humans. 40 patients undergoing coronary angioplasty of the left anterior descending (LAD) coronary artery (22 patients) or left circumflex (LC) artery (18 patients). Intracoronary and surface precordial ECGs were simultaneously recorded under baseline conditions and during angioplasty. Four different patterns of U-wave change were identified on the intracoronary ECG: change to positivity, no change, change to negativity, and biphasic change. The incidence of each pattern was similar in the two groups (LAD v LC groups, 23% v 39%; 23% v 17%; 41% v 44%; 13% v 0%, respectively). The intracoronary ECG was more sensitive than the surface ECG for detecting U-wave changes (intracoronary v surface ECG: LAD group, 77% v 55%; LC group, 83% v 28%). A study of the correlation between intracoronary and surface precordial ECGs showed that in patients who had U-wave changes in their intracoronary ECG (17 LAD and 15 LC patients) 65% of the LAD group but only 6% of the LC group had primary U-wave changes in the surface precordial ECG, and that 27% of the LC patients had reciprocal U-wave changes in the right to central precordial ECG. These results provide fundamental information for an understanding of the correlation between U-wave changes in the epicardial and surface pre-cordial ECGs during myocardial ischaemia in humans. As well as the primary U-wave changes seen in many of those with anterior myocardial ischaemia, some of those with posterior myocardial ischaemia had reciprocal U-wave changes in their surface precordial ECGs.

Myocardial Bridging: Surgical Technique and Operative Results

We report a case of a 37-year-old symptomatic male with anterior myocardial ischemia. Coronary angiography demonstrated systolic obstruction of the midportion of the left anterior descending coronary artery due to myocardial bridging. The patient was treated with a supra-arterial myotomy. Two years postoperatively, the patient is without evidence of myocardial ischemia. Angiography, 2 years postoperatively, shows no evidence of systolic narrowing of the left anterior descending coronary artery.

Revascularization of the internal mammary artery after coronary artery bypass grafting

Symptomatic anterior myocardial ischemia as a result of stenosis at the origin of the left internal mammary artery developed in a patient who underwent prior coronary artery bypass grafting using the left internal mammary artery as a conduit. Successful revascularization of the left anterior descending coronary artery was achieved using a reversed saphenous vein bypass graft from the left common carotid artery to the proximal internal mammary artery. This approach provided myocardial revascularization and avoided reoperative median sternotomy.

Effects of peroneal nerve stimulation on hypothalamic stimulation-induced ventricular arrhythmias in rabbits

We tested the hypothesis that peripheral afferent nerve stimulation decreases the incidence of ventricular arrhythmias induced by central nervous system stimulation. The hypothalamus in each of 24 anesthetized rabbits (12 with anterior myocardial ischemia) was electrically stimulated for 10 s with 10-min intervals between each of six consecutive stimulation episodes. The left peroneal nerves were electrically stimulated for 15 min beginning 5 min after the second hypothalamic stimulation episode in six ischemic and six nonischemic rabbits. Cardiac rhythm was monitored with the electrocardiogram lead I and atrial and ventricular electrograms. Hypothalamic stimulation alone induced ventricular arrhythmias [mean no. of arrhythmic beats occurring during 3rd and 4th hypothalamic stimulation episodes: nonischemic animals, 20 +/- 8; ischemic animals, 62 +/- 41 (P < 0.05 by unpaired t-test)]. Peroneal nerve stimulation reduced the number of arrhythmic beats induced by hypothalamic stimulation in nonischemic animals (6 +/- 5; P < 0.05 vs. without peroneal stimulation) and prevented an increase in arrhythmic beats during ischemia (21 +/- 16). Thus peripheral nerve stimulation decreased the number of ventricular arrhythmic beats induced by repeated hypothalamic stimulation in both ischemic and normal rabbit hearts and may be important in the prevention of arrhythmias in patients.

MR spectroscopy of the human heart: the status and the challenges.

Noninvasive measurements of high-energy phosphate metabolism in the anterior myocardium of heart patients are now possible with image-guided, localized nuclear magnetic resonance (MR) spectroscopy. The results, reviewed herein, are largely consistent with those of prior animal studies. Quantification with phosphorus-31 MR yields normal phosphocreatine (PCr) and adenosine triphosphate (ATP) concentrations of about 11 and 6 mumol per gram wet weight, respectively, with a PCr/ATP ratio of around 1.8. Studies of patients with hypertrophic and dilated cardiomyopathy, left ventricular hypertrophy, valve disease, transplanted hearts, myocardial infarction, or reversible ischemia reveal abnormalities in the PCr/ATP ratio and/or the metabolite concentrations. Differences in reported findings for cardiomyopathies might be attributable to statistical sensitivity and the presence of heart failure. The technique might find use in the clinic for identifying failure when other factors complicate diagnosis. The PCr/ATP ratio is often reduced in transplanted hearts but is not a reliable predictor of histologic rejection involving myocyte necrosis. In myocardial infarction, metabolite levels may be reduced while the remaining PCr and ATP signals likely reflect surrounding surviving tissue. Stress-test studies of anterior myocardial ischemia produce transient reductions in the PCr/ATP ratio, which appear to be specific for ischemic disease. This may lead to a new way of assessing ischemia, particularly if the technology can gain access to a larger portion of the heart. Cardiac spectroscopy with nuclei other than P-31 shows promise.