Impacts of nicorandil on infarct myocardium in comparison with nitrate: assessed by cardiac magnetic resonance imaging.

In this pilot study, we compared the infarct and edema size in acute myocardial infarction (MI) patients treated by nicorandil with those treated by nitrate, using cardiac magnetic resonance (CMR) imaging. Fifty-two acute MI patients who underwent emergency percutaneous coronary intervention (PCI) were enrolled, and were assigned to receive nicorandil or nitrate at random just before reperfusion. For the assessment of infarct and edema areas, short-axis delayed enhancement (DE) and T2-weight (T2w) CMR images were acquired 6.1 ± 2.4 days after the onset of MI. A significant correlation was observed between the peak creatinine kinase (CK) level and the infarct size on DE CMR (r = 0.62, p < 0.05), as well as the edema size on T2w CMR (r = 0.70, p < 0.05) in patients treated by nicorandil (28 patients). A similar correlation was seen between the peak CK level and the infarct size on DE CMR (r = 0.84, p < 0.05), as well as the edema size on T2w CMR (r = 0.84, p < 0.05) in patients treated by nitrate (24 patients). The maximum CK level was significantly lower in patients treated by nicorandil rather than nitrate (1991 ± 1402, 2785 ± 2121 IU/L, respectively, p = 0.03). Both the edema size on T2w CMR and the infarct size on DE CMR were significantly smaller in patients treated by nicorandil rather than nitrate (17.7 ± 9.9, 21.9 ± 13.7 %; p = 0.03, 10.3 ± 6.0, 12.7 ± 6.9 %, p = 0.03, respectively). The presence and amount of microvascular obstruction were significantly smaller in patients treated by nicorandil rather than nitrate (39.2, 64.7 %; p = 0.03; 2.2 ± 1.3, 3.4 ± 1.5 cm(2); p = 0.02, respectively). Using CMR imaging, we demonstrated that the complementary use of intravenously and intracoronary administered nicorandil during PCI favorably acts more on the damaged myocardium after MI than nitrate. We need a further powered prospective study on the use of nicorandil.

Diagnostic usefulness of the oedema-infarct ratio to differentiate acute from chronic myocardial damage using magnetic resonance imaging.

OBJECTIVES: To differentiate acute from chronic damage to the myocardium in patients with myocardial infarction (MI) using DE and T2w MR. METHODS: Short-axis T2w and DE MR images were acquired twice after the onset of MI in 36 patients who successfully underwent emergency coronary revascularisation. The areas of infarct and oedema were measured. The oedema-infarct ratio (O/I) of the left ventricular area was calculated by dividing the oedema by the infarct area. RESULTS: The oedema size on T2w MR was significantly larger than the infarct size on DE MR in the acute phase. Both the oedema size on T2w MR and the infarct size on DE MR in the acute phase were significantly larger than those in the chronic phase. The O/I was significantly greater in the acute phase compared with that in the chronic phase (P < 0.05). An analysis of relative cumulative frequency distributions revealed an O/I of 1.4 as a cut-off value for differentiating acute from chronic myocardial damage with the sensitivity, specificity, and accuracy of 85.1%, 82.7% and 83.9%, respectively. CONCLUSION: The oedema-infarct ratio may be a useful index in differentiating acute from chronic myocardial damage in patients with MI. KEY POINTS: MR can differentiate reversible from irreversible myocardial damage after myocardial infarction. MR is a useful modality to noninvasively differentiate the infarct stages. The O/I is an important index to decide therapeutic strategies.

Relation of plasma catecholamine levels with pulse wave velocity in hypertensive patients compared with normotensive subjects.

Although the circadian variation of catecholamine has been reported, that of the pulse wave velocity (PWV) has not. Brachial ankle (ba) PWV is associated with well-established indices of central stiffness. It is not known whether arterial stiffness is associated with catecholamine. The aim of the present study was to evaluate the changes in baPWV and those on the plasma epinephrine and norepinephrine levels in the morning and evening in hypertensive patients (HPs) and normotensive subjects (NSs). The baPWV and blood pressure (BP) were measured in 14 NSs (14 males, 39 ± 5 years) and 10 HPs (9 males and 1 female, 55 ± 13 years) at 06:00 h, noon, 18:00 h, and midnight, respectively. The plasma epinephrine and norepinephrine levels were measured in 14 NSs and 5 HPs at 06:00 h and 18:00 h, respectively. There was no significant difference in BPs at 06:00 h, noon, 18:00 h, and midnight in either NSs or HPs. The baPWV at 06:00 h was significantly lower than that at noon, 18:00 h, and midnight in NSs (P = 0.01, 0.04, and 0.0008, respectively). The plasma epinephrine and norepinephrine levels at 06:00 h were markedly lower than those at 18:00 h in NSs (P = 0.002 and 0.003, respectively). There were no significant changes in the baPWV of HPs at 06:00 h, noon, 18:00 h, or midnight. The plasma epinephrine and norepinephrine levels at 06:00 h were notably lower than those at 18:00 h in HPs (P = 0.004 and 0.01, respectively). Only NSs showed a significant reduction in the baPWV with a decrease in the plasma catecholamine levels in the morning, suggesting that the baPWV of NSs may be correlated with the variation of the plasma catecholamine levels.

Changes with age in left ventricular function and volumes at rest and postexercise in postmenopausal women.

OBJECTIVES: In postmenopausal women, it has been reported that the plasma estrogen levels diminish immediately after menopause, and that this phenomenon affects left ventricular (LV) function and volumes. However, the effects of age on LV function and volumes for a relatively short period in the postmenopausal women remain to be established. Electrocardiographically gated-myocardial single-photon emission computed tomography (SPECT) has recently provided accurate estimations of perfusion, cardiac systolic and diastolic functions. We investigated the age-related changes in LV function and volumes in postmenopausal women using electrocardiographically gated-myocardial scintigraphy. METHODS: Twenty-two consecutive healthy postmenopausal women (mean age of 63.8 +/- 9.4 years, from 42 to 77 years) without cardiac disease underwent stress/rest technetium-99m tetrofosmin gated-myocardial SPECT with 16 frames per cardiac cycle at baseline and follow-up (1.0 +/- 0.3 years later). LV ejection fraction (LVEF) and LV volumes were calculated by QGS software. Fourier series were retained for the analysis of the volume curve. From this volume curve, we derived the following diastolic indices: peak filling rate (PFR) and time to PFR (TPFR). RESULTS: End-systolic volume index (ESVI) significantly decreased at postexercise (p = 0.02) and tended to decrease at rest (p = 0.06) from the baseline to the follow-up study. LVEF significantly increased at both postexercise (p = 0.01) and rest (p = 0.03) from the baseline to the follow-up study. The TPFR at rest tended to be prolonged from the baseline to the follow-up study (p = 0.07). The absolute increase in LVEF at postexercise tended to decrease with age [4.8% (50s) vs. 3.4% (60s) vs. 1.2% (70s)]. CONCLUSIONS: An age-related change in cardiac performance is apparent at an approximately 1 year follow-up in postmenopausal women. In particular, the increase in LV systolic function tends to show the greatest value in the 50s subjects among the 3 generations.

Diagnostic usefulness of postexercise systolic blood pressure response for detection of coronary artery disease in patients with echocardiographic left ventricular hypertrophy.

BACKGROUND: Although exercise-induced electrocardiographic ST segment changes are used to detect coronary artery disease (CAD), their diagnostic value is markedly decreased in patients with left ventricular (LV) hypertrophy. There have been no reports concerning postexercise systolic blood pressure (SBP) response in patients with ultrasound echocardiographic (UCG) LV hypertrophy and CAD. METHODS: Sixty-six patients with both UCG-LV hypertrophy (LV mass index 134 g/m2 or greater for men or 110 g/m2 or greater for women) and positive ST depression of at least 0.1 mV during treadmill exercise testing were studied. Coronary cineangiograms showed normal coronary arteries in 19 patients (group 1) and significant CAD in 47 patients (group 2). The SBP ratio was calculated by dividing the SBP 3 min after exercise (3 min SBP) by the SBP at peak exercise (peak SBP). RESULTS: There were no significant differences between the two groups in LV mass index, SBP at rest, exercise duration, ST depression (at rest and exercise-induced) or 3 min SBP. However, the SBP ratio was significantly higher in group 2 compared with group 1 (0.87+/-0.11 versus 1.01+/-0.18; P=0.004). Analysis of relative cumulative frequency distributions revealed an SBP ratio of 0.92 as the cutoff point for distinguishing a UCG-LV hypertrophy patient with CAD from one without CAD. The sensitivity, specificity and accuracy with an SBP ratio of 0.92 and an ST segment depression of at least 0.1 mV on treadmill exercise testing for detecting CAD in patients with UCG-LV hypertrophy were 77%, 74% and 76%, respectively. CONCLUSION: These findings suggest that the ratio of early post-exercise SBP to peak exercise SBP may be diagnostically useful in detecting CAD in patients with positive ST depression during an exercise test and UCG-LV hypertrophy.

Paclitaxel-induced interstitial pneumonia after drug-eluting stent implantation: report of a fatal case.

We report a case of paclitaxel-eluting stent implantation in an angina patient who developed interstitial pneumonia a few days afterward, and succumbed to fatal respiratory dysfunction despite corticosteroid therapy. Paclitaxel is an anti-neoplastic agent currently used as a coating substance for coronary stents to reduce the rate of restenosis. Pulmonary toxicity related to paclitaxel is not very common; however, this adverse event may on occasion be lethal. Although the efficacy and safety of drug-eluting stents for the treatment of ischemic heart disease is well established, physicians should keep in mind that paclitaxel-eluting stents have the potential to cause interstitial pneumonia.

Increase in electrocardiographic R-waves after revascularization in patients with acute myocardial infarction.

BACKGROUND: The physiological mechanism of the increase in the electrocardiographic (ECG) R-wave voltage after revascularization in patients with acute myocardial infarction (MI) needs to be elucidated. METHODS AND RESULTS: One hundred and thirty-eight MI patients (83: anterior MI, 45: inferior MI, 10: lateral MI) underwent ECG and echocardiography in both the acute and subacute phases after emergency revascularization, as well as a resting thallium-201/iodine-123 15-p-iodophenyl-3-(R,S)-methyl pentadecanoic acid myocardial scintigraphy in the acute phase. The total sum of the R-wave voltage (SigmaR) was calculated over multiple leads on ECG for each infarcted lesion. Scintigraphic defect on each tracer was expressed as the percentage (%) defect of the total left ventricular (LV) myocardium. The % defect-discordance on both images in the acute phase and the % increase in SigmaR and the absolute increase in LV ejection fraction from the acute to the subacute phase (DeltaEF) were also calculated. The SigmaR in the subacute phase was significantly greater than that in the acute phase (p<0.0001). The % increase in SigmaR significantly correlated with the DeltaEF (r=0.57, p<0.0001). The % increase in SigmaR also correlated with the % defect-discordance (r=0.68, p<0.0001). CONCLUSIONS: The increase in the ECG R-wave voltage reflects not only the improvement in myocardial perfusion but also the presence of salvaged myocardium after revascularization in acute MI patients.

Cardiac sympathetic dysfunction correlates with abnormal myocardial contractile reserve in dilated cardiomyopathy patients.

OBJECTIVES: We investigated the relationship between iodine-123-metaiodobenzylguanidine (123I-MIBG) findings and myocardial contractile reserve in patients with mild to moderate dilated cardiomyopathy (DCM). BACKGROUND: Little is known regarding the relationship between cardiac sympathetic nervous function and myocardial contractile reserve in DCM. METHODS: Twenty-four DCM patients who showed sinus rhythm underwent echocardiography, biventricular catheterization, and myocardial 123I-MIBG scintigraphy. Left ventricular (LV) pressures were measured using a micromanometer-tipped catheter. The myocardial contractile function (LV dP/dt(max)) was determined at rest and during atrial pacing. The messenger ribonucleic acid (mRNA) expressions of intracellular Ca2+-regulatory proteins were analyzed by real-time quantitative reverse transcription-polymerase chain reaction. Myocardial 123I-MIBG accumulation was quantified as a heart-mediastinum ratio (HMR). RESULTS: A significant correlation was observed between the delayed 123I-MIBG HMR and the percentage change in LV dP/dt(max) from the baseline to the peak or critical heart rate (r = 0.64; p < 0.001). The delayed 123I-MIBG HMR was significantly lower in patients showing a worsening change in LV dP/dt(max) than in those showing a favorable change (p < 0.005). The maximum LV dP/dt(max) during pacing and the sarcoplasmic reticulum Ca2+-ATPase (SERCA2) mRNA levels were significantly more reduced in patients with a delayed HMR < or =1.8 than in those with a delayed HMR >1.8 (p < 0.05, respectively). CONCLUSIONS: Abnormal myocardial 123I-MIBG accumulation is related to an impaired myocardial contractile reserve and down-regulation of SERCA2 mRNA in DCM. Myocardial 123I-MIBG scintigraphy can be useful in noninvasively evaluating myocardial contractile reserve in patients with mild to moderate DCM.