Left ventricular systolic dyssynchrony is a predictor of cardiac remodeling after myocardial infarction.

OBJECTIVES: We sought to determine whether early assessment of left ventricular (LV) dyssynchrony by tissue Doppler imaging may predict progressive ventricular enlargement and cardiac dysfunction after acute myocardial infarction (MI). METHODS: Forty-seven patients (mean age 59.9 +/- 11.6 years) with normal QRS duration underwent tissue Doppler imaging and contrast-enhanced cardiac magnetic resonance imaging (Ce-MRI) at days 2 to 6, 3 months, and at 1 year after the index MI. Systolic dyssynchrony index (Ts-SD) was calculated from 12 LV segments, and infarct size (IS) by Ce-MRI. RESULTS: The remodeling group (n = 16) (defined as an increase in end-systolic volume > or =10% between 1 year and baseline) had greater initial IS (27.2 +/- 9.6 vs 13.7 +/- 4.1%, P < .001) and Ts-SD (50.9 +/- 12.8 vs 33.6 +/- 7.7 milliseconds, P < .001) than nonremodeling group (n = 31). At 1 year, the remodeling group had progressive increase in Ts-SD and decrease in LV ejection fraction (57.3 +/- 18.5 and 36.0 +/- 7.6%, respectively; both P < .05 vs baseline). Both Ts-SD (odds ratio 1.19 [1.07-1.32], P = .001) and IS (odds ratio 1.65 [1.19-2.29], P = .003) were shown to be independent predictors of progressive LV remodeling. A cutoff value of Ts-SD > or =45 milliseconds predicted LV remodeling at 1 year (sensitivity 90.5%, specificity 90.9%, Area-under-curve 0.907) (P = .0005). CONCLUSIONS: Left ventricular systolic dyssynchrony is a newly identified predictor of chronic LV remodeling after acute MI, which is independent and incremental to conventional assessment and IS as measured by Ce-MRI.

Diagnostic dilemma in a middle-aged man with heart failure.

We report a middle-age man presented with shortness of breath. Echocardiography revealed globally hypokinetic LV with poor function. Coronary angiograms showed no obstructive coronary artery lesions but multiple coronary fistulae to pulmonary artery without significant left to right shunt. Cardiac magnetic resonance imaging demonstrated normal myocardial perfusion and absence of myocardial scarring. His condition improved with medications with fistulae left untreated. This case illustrates the importance of functional assessment of a rare clinical condition (coronary fistula) in patients with common clinical presentation (congestive heart failure) prior to definitive treatment.

Aldosterone receptor antagonism induces reverse remodeling when added to angiotensin receptor blockade in chronic heart failure.

OBJECTIVES: The objective of this study was to determine if adding spironolactone to an angiotensin II receptor blocker improves left ventricular (LV) function, mass, and volumes in chronic heart failure. BACKGROUND: Add-on spironolactone therapy substantially improves clinical outcomes among patients with severe heart failure (HF) on standard therapy. However, the value of combining spironolactone with an angiotensin II receptor blocker on LV reverse remodeling in mild-to-moderate systolic HF is unclear. METHODS: Fifty-one systolic HF patients with left ventricular ejection fraction (LVEF) <40% were randomly assigned to receive 1-year treatment of candesartan and spironolactone (combination group) or candesartan and placebo (control group). Reverse remodeling was assessed by serial cardiac magnetic resonance imaging and echocardiographic tissue Doppler imaging (TDI). RESULTS: There were significant improvements in LVEF (35 +/- 3% vs. 26 +/- 2%, p < 0.01) and reduction of LV end-diastolic volume index (121 +/- 16 ml/m2 vs. 155 +/- 14 ml/m2, p = 0.001), end-systolic volume index (88 +/- 17 ml/m2 vs. 120 +/- 15 ml/m2, p < 0.0005), and LV mass index (81 +/- 6 g/m2 vs. 93 +/- 6 g/m2, p = 0.002) in the combination group at 1 year. In addition, there was significant increase in peak basal systolic velocity and strain by TDI, decrease in index of filling pressure, and increase in cyclic variation integrated backscatter. In the control group, there were no significant changes in all these parameters after 1 year. CONCLUSIONS: The addition of spironolactone to candesartan has significant beneficial effects on LV reverse remodeling in patients with mild-to-moderate chronic systolic HF.

Strain rate imaging differentiates transmural from non-transmural myocardial infarction: a validation study using delayed-enhancement magnetic resonance imaging.

OBJECTIVES: The aim of this study was to determine if strain rate imaging (SRI) correlates with the transmural extent of myocardial infarction (MI) measured by contrast-enhanced magnetic resonance imaging (Ce-MRI). BACKGROUND: Identification of the transmural extent of myocardial necrosis and degree of non-viability after acute MI is clinically important. METHODS: Tissue Doppler echocardiography with SRI and Ce-MRI were performed in 47 consecutive patients with a first acute MI between days 2 and 6 and compared to 60 age-matched healthy volunteers. Peak myocardial velocities and peak myocardial deformation strain rates were measured. Location and size of the infarct zone was confirmed by Ce-MRI using the delayed enhancement technique with a 16-segment model. RESULTS: Contrast-enhanced MRI identified transmural infarction in 21 patients, non-transmural infarction in 15 (mean transmurality of infarct 72.3 +/- 10.6%), and another 11 patients with subendocardial infarction (<50% transmural extent of the left ventricular wall). Peak systolic strain rate (SRs) of the transmural infarction segments was significantly lower compared to normal myocardium or with non-transmural infarction segments (both p < 0.0005). A cutoff value of SRs >-0.59 s(-1) detected a transmural infarction with high sensitivity (90.9%) and high specificity (96.4%), and -0.98 s(-1) >SRs >-1.26 s(-1) distinguished subendocardial infarction from normal myocardium with a sensitivity of 81.3% and a specificity of 83.3%. CONCLUSIONS: Peak myocardial deformation by SRI can differentiate transmural from non-transmural MI, and it allows noninvasive determination of transmurality of the scar after MI and thereby the extent of non-viable myocardium.

Left ventricular systolic asynchrony after acute myocardial infarction in patients with narrow QRS complexes.

BACKGROUND: The aim of the study was to assess the degree of left ventricular (LV) asynchrony after myocardial infarction (MI) in patients with a narrow QRS complex using tissue Doppler imaging (TDI) and correlate this with the site and extent of the infarction measured by contrast-enhanced magnetic resonance imaging (Ce-MRI). METHODS: Echocardiography with TDI and Ce-MRI was performed within 6 days of acute MI in 47 patients and compared with 69 age-matched healthy volunteers. Regional myocardial velocities were assessed in 12 segments, and the corresponding systolic velocity (Sm), early diastolic velocity (Em), as well as the time to peak Sm (Ts) and time to peak Em (Te) were measured. To assess LV synchronicity, SDs of Ts (Ts-SD) and Te (Te-SD) of all 12 segments were computed. Location and size of infarct were confirmed by Ce-MRI with a 16-segment model. RESULTS: All the patients had a normal QRS complex duration. The Ts-SD was significantly prolonged in the MI group when compared with controls (42.2 +/- 13.7 vs 18.0 +/- 7.0 milliseconds, P < .001). The Ts-SD was longer in patients with anterior than inferior MI (46.8 +/- 13.9 vs 34.6 +/- 8.5 milliseconds, P = .002). Stepwise multiple regression analysis revealed that infarct size was the main independent predictor of systolic asynchrony ( B = 0.79, 95% CI 0.75-1.23, P < .001). Asynchrony was not related to the transmurality of the infarction. CONCLUSIONS: Myocardial infarction has a significant impact on LV synchronicity even in those with a narrow QRS complex. The degree of LV systolic asynchrony is mainly determined by the infarct size and not transmurality.

Effect of N-acetylcysteine for prevention of contrast nephropathy in patients with moderate to severe renal insufficiency: a randomized trial.

BACKGROUND: The effect of N-acetylcysteine (NAC) to prevent contrast nephropathy (CN) in patients with moderate to severe renal insufficiency undergoing coronary angiography or interventions is not clear. METHODS: This is a prospective, open-label, randomized, controlled trial. Ninety-one consecutive patients with a serum creatinine level of 1.69 to 4.52 mg/dL (149 to 400 micromol/L) undergoing coronary procedures were recruited and randomly assigned to administration of either oral NAC, 400 mg, thrice daily the day before and day of the contrast procedure (the NAC group) or no drug (the control group). Serum creatinine was measured before and 48 hours after contrast exposure. The primary end point of this study was the development of CN, defined as an increase in serum creatinine concentration of 0.5 mg/dL or greater (> or =44 micromol/L) or a reduction in estimated glomerular filtration rate (GFR) of 25% or greater of the baseline value 48 hours after the procedure. RESULTS: There were no significant differences between the 2 groups (46 patients, NAC group; 45 patients, control group) in baseline characteristics or mean volume of contrast agent administered. Six patients (13.3%) in the control group and 8 patients (17.4%) in the NAC group developed CN (P = 0.8). Serum creatinine levels increased from 2.27 +/- 0.54 to 2.45 +/- 0.65 mg/dL (201 +/- 48 to 217 +/- 57 micromol/L; P = 0.003) in the NAC group and 2.37 +/- 0.61 to 2.40 +/- 0.70 mg/dL (210 +/- 54 to 212 +/- 62 micromol/L; P = 0.6) in the control group. The increase in serum creatinine levels between the 2 groups had no difference (P = 0.7). Estimated GFR decreased from 30.3 +/- 8.4 to 28.1 +/- 8.4 mL/min (P = 0.01) in the NAC group and 28.4 +/- 8.6 to 27.5 +/- 8.8 mL/min (P = 0.3) in the control group. The decline in estimated GFR between the 2 groups had no difference (P = 0.7). CONCLUSION: In the current study, oral NAC had no effect on the prevention of CN in patents with moderate to severe renal insufficiency undergoing coronary angiography or interventions. However, the sample size of our present study is small. Our findings highlight the need for a large-scale, randomized, controlled trial to determine the exact beneficial effect of NAC.

Homocysteine, endothelial dysfunction, and coronary artery disease: emerging strategy for secondary prevention.

Atherosclerosis is an important medical problem of the 21st century, but traditional risk factors could only account for 50% of the problem. Hyperhomocysteinemia is emerging as an independent atherosclerosis risk factor, associated with folate deficiency, renal failure, and relative deficiency of MTHFR (C677T polymorphism) or other enzymes depending on gender, age, and smoking status. Hyperhomocysteinemia has been reported to occur in 11-22% of western people, in 3-5% of normal asymptomatic Chinese subjects aged 18-70 years in Hong Kong, Macau, Sydney, and San Francisco, 23-36% of Chinese in Hong Kong with premature coronary artery disease, and 29% of a nonselective series of coronary subjects in Hong Kong. Evidence is accumulating that documents its associations with atherosclerosis disease in both case-control observations and prospective cohort studies, in vitro experiments, and in vivo experimental models in both animals and human subjects, as well as the successful improvement by homocysteine-lowering of endothelial function as surrogate atherosclerosis endpoints in asymptomatic human and coronary patients (secondary prevention). A number of large scale homocysteine-lowering trials are currently underway for stroke and heart attacks prevention. Collectively these trials will include more than 65,000 patients at high-risk for cardiovascular and stroke events, and should provide a reliable evidence-base for prevention.