Dual-phase multi-detector computed tomography assesses jeopardised and infarcted myocardium subtending infarct-related artery early after acute myocardial infarction.

OBJECTIVES: To investigate dual-phase multi-detector computed tomography (MDCT) for assessing extent and severity of jeopardised and infarcted myocardium subtended by infarct-related artery (IRA), and its indication for revascularisation after acute myocardial infarction (AMI). Designs, setting and PATIENTS: Prospective, single-centre study included 107 patients with uncomplicated post-AMI 3-7 days, who met criteria and underwent dual-phase 64-slice MDCT. IRA, culprit lesion and extent of jeopardised/infarcted myocardium were assessed by three-dimensional (3D) volume-rendered images with myocardium maps and computed tomography angiography (CTA), compared with stress-redistribution thallium-201 single-photon emission computed tomography (SPECT) plus conventional coronary angiography (CCA). MDCT-jeopardised score (severity of jeopardised myocardium) was defined as extent of jeopardised myocardium multiplied by the weighted factor dependent on culprit lesion severity compared with SPECT-SRS (summation of segmental reversible score). The IRA indication for revascularisation was evaluated by MDCT-jeopardised score plus CTA. SPECT-SRS > or =2 plus CCA-culprit lesion > or =50% was the standard reference. RESULTS: The presence of MDCT-delayed enhancement was found in 101 (94.4%) patients. The IRA and culprit lesion were identified in 99 (92.5%) patients by MDCT-myocardium maps plus CTA. The concordance between MDCT and SPECT for detecting infarcted myocardium was good (kappa = 0.702). The correlation between MDCT-jeopardised score and SPECT-SRS was 0.741. The correlation between CTA and CCA for culprit lesion severity was 0.85. The sensitivity, specificity, negative and positive predictive values of MDCT-jeopardised score > or =2.5 plus CTA for indicating revascularisation were 90.2%, 80.4%, 86.0% and 85.9%, respectively. CONCLUSIONS: Dual-phase MDCT has good accuracy for identifying IRA, and assessing infarcted and jeopardised myocardium for clinical relevance. It provides an alternative for triage and therapeutic planning in post-AMI.

Vascular stiffness in familial hypercholesterolaemia is associated with C-reactive protein and cholesterol burden.

BACKGROUND: Familial hypercholesterolaemia (FH) is characterized by very high serum cholesterol and premature coronary atherosclerosis. Arterial stiffness and atherosclerosis are two major underlying pathophysiologies of arterial disease that are predictive of future cardiovascular events. The aims of this study were to quantify atherosclerosis and arterial stiffness and to evaluate their relationship with high sensitive C-reactive protein (hs-CRP) and the level of exposure to high serum cholesterol in FH patients. MATERIALS AND METHODS: We measured traditional risk factors, hs-CRP, intima-media thickness (IMT) of carotid artery, and brachial-ankle pulse wave velocity (baPWV) in 35 heterozygous FH subjects and 17 healthy control subjects. Cholesterol-year score (CYS) was calculated to estimate the lifetime cholesterol burden in FH subjects. RESULTS: FH subjects had significantly elevated total cholesterol, low-density lipoprotein cholesterol, and carotid IMT compared with those without mutations. Among FH patients, the baPWV and carotid IMT were higher in cases with high cholesterol burden than those without. Similarly, the baPWV and carotid IMT were also higher in cases with elevated hs-CRP (> 1 mg L(-1)) than those without. Multiple linear regression analysis demonstrated CYS and hs-CRP were significant independent predictors of baPWV and IMT in FH patients. CONCLUSIONS: Both high cholesterol burden and vascular inflammation are not only associated with atherosclerosis, but also contribute to the development of arterial stiffness in FH patients. Early detection of hypercholesterolaemia in FH patients is warranted to prevent the untoward pathophysiologies.

Identification and characterization of novel low-density lipoprotein receptor mutations of familial hypercholesterolaemia patients in Taiwan.

BACKGROUND: Familial hypercholesterolaemia (FH) is an autosomal dominant disease associated with a very high risk of coronary vascular disease. The study objective was to identify patients with FH in Taiwan and characterize novel mutations. MATERIALS AND METHODS: Fifty-one patients with suspected FH living in Taiwan were screened for mutations in both the low-density lipoprotein (LDL) receptor and the apolipoprotein (apoB) genes using the multiplex polymerase chain reaction and exon-by-exon DNA sequencing technique. Functional consequences on LDL receptor activity were characterized in vitro for novel mutations and family pedigree was also analyzed. RESULTS: Thirteen different functional mutations in the LDL receptor gene and one mutation in the apoB gene were found in 21 patients. Among the 13 mutations in the LDL receptor gene, 10 were single-point missense mutations, one was a two-point mutation in the same allele, one was a non-sense mutation and one was a frame-shift mutation. There were three novel mutations, including two missense mutations (M510K and W512R) and one frame-shift mutation (1953 delTA mutation). The characterization of missense M510K retained 36.2% of the activity of the normal receptor. Conversely, frame-shift 1953 delTA and missense W512R led to defective proteins, with only 0-6% of normal receptor activity. CONCLUSIONS: The study identified 13 LDL receptor gene mutations and characterized three novel mutations causing FH in Taiwan. This facilitated a better understanding of FH among the Chinese population and may enable diagnosis of FH at the molecular level at a presymptomatic, early age.

Noninvasive single-beat determination of left ventricular end-systolic elastance in humans.

OBJECTIVES: The goal of this study was to develop and validate a method to estimate left ventricular end-systolic elastance (E(es)) in humans from noninvasive single-beat parameters. BACKGROUND: Left ventricular end-systolic elastance is a major determinant of cardiac systolic function and ventricular-arterial interaction. However, its use in heart failure assessment and management is limited by lack of a simple means to measure it noninvasively. This study presents a new noninvasive method and validates it against invasively measured E(es). METHODS: Left ventricular end-systolic elastance was calculated by a modified single-beat method employing systolic (P(s)) and diastolic (P(d)) arm-cuff pressures, echo-Doppler stroke volume (SV), echo-derived ejection fraction (EF) and an estimated normalized ventricular elastance at arterial end-diastole (E(Nd)): E(es(sb)) = [P(d) - (E(Nd(est)) x P(s) x 0.9)[/(E(Nd(est)) x SV). The E(Nd) was estimated from a group-averaged value adjusted for individual contractile/loading effects; E(es(sb)) estimates were compared with invasively measured values in 43 patients with varying cardiovascular disorders, with additional data recorded after inotropic stimulation (n = 18, dobutamine 5 to 10 microg/kg per min). Investigators performing noninvasive analysis were blinded to the invasive results. RESULTS: Combined baseline and dobutamine-stimulated E(es) ranged 0.4 to 8.4 mm Hg/ml and was well predicted by E(es(sb)) over the full range: E(es) = 0.86 x E(es(sb)) + 0.40 (r = 0.91, SEE = 0.64, p < 0.00001, n = 72). Absolute change in E(es(sb)) before and after dobutamine also correlated well with invasive measures: E(es(sb)): DeltaE(es) = 0.86 x DeltaE(es(sb)) + 0.67 (r = 0.88, p < 0.00001). Repeated measures of E(es(sb)) over two months in a separate group of patients (n = 7) yielded a coefficient of variation of 20.3 +/- 6%. CONCLUSIONS: The E(es) can be reliably estimated from simple noninvasive measurements. This approach should broaden the clinical applicability of this useful parameter for assessing systolic function, therapeutic response and ventricular-arterial interaction.

Significance of cardiac troponin I and creatine kinase release after coronary intervention.

BACKGROUND: Cardiac troponin I is a highly sensitive and specific marker for early detection of myocardial injury. Whether it can be used to monitor myocardial injury after coronary intervention is uncertain. This study was designed to measure the cardiac troponin I and creatine kinase (CK) after coronary intervention and investigate their clinical significance. METHODS: We measured cardiac troponin I and CK levels before intervention and 4 hours, 8 hours, 12 hours and 24 hours after apparently successful coronary intervention in 106 eligible patients. Nine patients were excluded due to missing data. We also followed up the clinical outcome to record major cardiac events (MACE). RESULTS: The frequency of cardiac troponin I increase after coronary intervention was higher than that of CK increase (40.2% vs 8.2%). The frequency of cardiac troponin I increase in the stent group was significantly higher than that in the PTCA group (49.2% vs 21.9%, p < 0.001). The frequency of cardiac troponin I increase was also higher than that of CK increase in patients with in-hospital events (58.8% vs 14.7%). CONCLUSIONS: Cardiac troponin I is more sensitive than creatine kinase in detecting myocardial injury after coronary intervention. The incidence of cardiac troponin I increase is significantly higher in patients undergoing stenting than in patients treated with balloon angioplasty only. The cardiac troponin I increase is more highly correlated with in-hospital events than is creatine kinase.

Randomized, double-blind comparison of irbesartan and enalapril for treatment of mild to moderate hypertension.

BACKGROUND: Irbesartan is a newly developed angiotensin II receptor antagonist. Its antihypertensive efficacy and safety in Taiwanese patients with mild to moderate hypertension remains to be determined. METHODS: This was a multicenter, double-blind, randomized, parallel group study. One hundred and sixteen patients from three centers were enrolled. After a placebo lead-in period of 14 days, 55 patients (24-75 years-of-age) who had a mean seated diastolic blood pressure of 95 to 110 mmHg were randomized to once-daily treatment with irbesartan 150 mg or enalapril 10 mg. Doses were doubled at week 4 if trough seated diastolic blood pressure was 90 mmHg or more. Trough blood pressure was measured at zero, two, four and eight weeks of treatment. RESULTS: Both treatments lowered blood pressure with no significant difference in efficacy between treatment groups. Irbesartan 150 mg to 300 mg provided reductions in trough seated systolic and diastolic blood pressures at week 8 of -16.5 mmHg and -7.2 mmHg, respectively, with 36% of patients having a favorable response. Similarly, enalapril 10 mg to 20 mg reduced systolic and diastolic blood pressure by -10.6 mmHg and -5.0 mmHg, respectively, with a response rate of 43%. Headache, malaise and dizziness were the major adverse reactions observed in both groups. The incidence of drug-related cough was significantly higher with enalapril (18%) than with irbesartan (0%). CONCLUSIONS: Irbesartan 150 mg to 300 mg once daily was as effective in lowering blood pressure as enalapril 10 mg to 20 mg once daily. Both irbesartan and enalapril were well tolerated, while there was a significantly lower incidence of cough with irbesartan compared with enalapril.

Results of coronary stenting after delayed angioplasty of the culprit vessel in patients with recent myocardial infarction.

Little information is available concerning the effect of late coronary stenting in patients with recent myocardial infarction, especially long-term results. We retrospectively reviewed our results of 57 stent placements in 52 consecutive patients who received stents at an infarct-related lesion 24 hr to 30 days after an acute myocardial infarctions (median, 14 days). The average age was 67 years; 90% were male. Two patients who suffered from acute stent thrombosis received revascularization again and two early deaths were due to refractory cardiogenic shock before discharge. Mean patient clinical follow-up was 18.3 +/- 6.5 months. There were 1 subacute stent thrombosis, 1 cardiogenic death, and 10 patients (20.8%) in total suffering from angina class II to IV. Angiographic follow-up was performed in 36 patients (80%) at a mean of 7.5 +/- 3.1 months. Of these 36 patients, only 1 (3% of the total population undergoing follow-up angiography) had reocclusion at follow-up, but restenosis existed in 18 patients (50%). We conclude that there is still relatively high incidence of angiographic recurrence that is often silent in long-term follow-up, though the long-term result of late stenting in recent MI is low incidence of reocclusion.