A dangerous bridge: myocardial infarction due to myocardial bridging in left ventricular hypertrophy

A 63-year-old woman with a history of hypertension presentedto the coronary care unit with a subacute anterior wall myocardialinfarction (MI). She reported of initial left-sided chest pain,dyspnoea, and weakness 18 h before hospital admission, duringa long-distance     

Clinical significance and prognostic importance of left ventricular hypertrophy in non-Q-wave acute myocardial infarction

Left ventricular (LV) hypertrophy is known to be an independent risk factor for cardiac death, but its significance in non-Q-wave acute myocardial infarction (AMI) has not been assessed previously. In a randomized diltiazem-placebo-controlled therapeutic trial of non-Q-wave AMI confirmed by creatine kinase-MB (CK-MB), 126 of 544 patients (23%) exhibited LV hypertrophy using standard voltage criteria. Compared to patients without LV hypertrophy, patients with LV hypertrophy were significantly older (65 vs 60 years, p less than 0.0001) and had smaller peak adjusted CK levels (490 +/- 376 vs 666 +/- 726 IU/liter, p less than 0.001) than patients without LV hypertrophy. Patients with and without LV hypertrophy did not differ significantly in acute mortality during hospitalization, progression to Q waves, reinfarction by CK-MB criteria or angina associated with transient electrocardiographic changes. Compared with patients without LV hypertrophy, those patients with non-Q-wave AMI and LV hypertrophy had a 2-fold higher incidence of reinfarction (24 vs 12%, p less than 0.005) and death (19 vs 9%, p = 0.044) during the first year of follow-up. Multivariate regression analysis revealed that the relative risk of death and reinfarction during the initial year after AMI was increased by a factor of 1.7 and 2.1 among patients with LV hypertrophy, respectively. It was therefore concluded that, although patients with LV hypertrophy and non-Q-wave AMI have smaller enzymatic infarcts and the same short-term prognosis as do patients without LV hypertrophy, their reinfarction and mortality rates are significantly increased during the first year of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)     

Midwall myocardial shortening in athletic left ventricular hypertrophy

BACKGROUND: Patients with pathological left ventricular hypertrophy have depressed midwall systolic shortening in spite of normal indices of left ventricular chamber function and a reduced midwall function has been observed to be an independent predictor of cardiovascular risk. Whether midwall shortening is depressed in physiological hypertrophy is unknown. METHODS: Forty-two subjects, 27 athletes and 15 age- and sex-matched normal control subjects (group 1) were studied. The athletes were divided into those with eccentric hypertrophy (group 2) and those with concentric hypertrophy (group 3). Systolic left ventricular function was assessed at the midwall and endocardium using two-dimensional echocardiography in all subjects. RESULTS: Left ventricular mass index was significantly greater in both athletic groups than in controls (group 1, 101+/-5.8 g/m(2), group 2, 141+/-11.1*, group 3, 155+/-5.8*; *P<0.01 compared with group 1). Left ventricular systolic function assessed at the endocardium was similar among all three groups (ejection fraction: group 1, 66.2+/-2.38, group 2, 66.8+/-1.44, group 3, 63.7+/-1.66%; endocardial fractional shortening: group 1, 37.1+/-1.71, group 2, 37.6+/-1.13, group 3, 35.1+/-1.25%). However, fractional shortening at the midwall was reduced in the concentric hypertrophy athletes compared with the other two groups (midwall fractional shortening: group 1, 21.9+/-1.1, group 2, 21.9+/-0.86, group 3, 18.4+/-0.96*%; P<0.05 compared with groups 1 and 2). CONCLUSION: Subjects with physiological concentric hypertrophy have depressed midwall fractional shortening. This suggests that the observed discrepancy between midwall and endocardial shortening in patients with left ventricular hypertrophy is likely to be a function of the geometry and not necessarily a reflection of pathology within the myocardium.     

Progressive left ventricular hypertrophy after withdrawal of long-term ACE inhibition following experimental myocardial infarction

BACKGROUND: Although discontinuation of chronic ACE inhibitor (ACEi) therapy after myocardial infarction (MI) is common in clinical practice, some clinical studies reported an increased incidence of ischemia-related events after withdrawal. To further address this issue, we assessed hemodynamic, neurohormonal and vascular consequences of withdrawing long-term ACEi treatment after experimental MI. METHODS: Rats were subjected to coronary ligation to induce MI, and received quinapril (15 mg/kg/day) from 2 weeks to 14 months post-MI. Subsequently, surviving rats were randomized to sacrifice at 0, 4, and 6 weeks after ACEi withdrawal. Rats were studied for signs of heart failure, hemodynamics and cardiac function, neurohormones, and vascular edothelial function. RESULTS: After discontinuation of ACEi treatment, plasma aldosterone levels increased between 0-4 weeks without further increment thereafter, suggesting persistent RAAS activation. Acetylcholine-induced aortic relaxation was impaired at 4 and 6 weeks, indicating rapid and sustained development of endothelial vasodilator dysfunction after withdrawal. Moreover, 24% of the rats developed heart failure signs (edema, dyspnea), and 3 rats died, all within 4 weeks after withdrawal. Significantly increased N-ANP levels and lung weights at 4, but not at 6 weeks suggest a transient volume overload. Finally, LV/body weight ratios significantly increased between 0-4 as well as 4-6 weeks, indicating progressive LV hypertrophy. CONCLUSIONS: The observed alterations after withdrawing long-term post-MI quinapril treatment in the present study may account for an increased risk for ischemic events. Thus, our findings highlight the potentially harmful effects associated with abrupt discontinuation of long-term post-MI ACE inhibition, and imply careful clinical consideration in this matter.     

Post myocardial infarction left ventricular pseudoaneurysm

Left ventricular pseudoaneurysm is a rare yet serious and challenging complication of myocardial infarction that requires a high index of suspicion as the clinical presentation is highly variable. We present a case of post infarction thrombosed left ventricular pseudoaneurysm in a patient who presented with non-specific complaints months after the initial cardiac injury. Multimodality imaging helped in characterizing the pseudoaneurysm and planning for definite therapy.     

急性心肌梗死与左室重构

急性心肌梗死(AMI)后左室发生细胞学,分子学及细胞间质的变化,进而引起左室在大小、形态、组织结构和功能状态的改变,此即目前许多研究所提及的AMI后的左室重构.AMI后左室的重构贯穿于整个病程的始终,成为影响AMI患者近远期预后的主要原因之一.     

Prognostic value of left ventricular hypertrophy and geometry in patients with a first, uncomplicated myocardial infarction

BACKGROUND: The prognostic impact of left ventricular (LV) geometry on cardiovascular risk for patients with a first, uncomplicated acute myocardial infarction (AMI), and echocardiographic ejection fraction > or =50% has not been well described. METHODS AND RESULTS: Accordingly, 111 AMI consecutive patients (mean age 59.3+/-10 years) performed echocardiographic examination at predischarge. LV mass was calculated by means of Devereux's formula and subsequently indexed by body surface area. Fifty-three patients had LV hypertrophy and 58 patients had normal LV mass. The two groups were homogeneous for demographic, clinical and angiographic variables as well as for the incidence of residual ischemia on predischarge stress testing. During follow-up period there were 24 cardiac events (cardiac death, unstable angina and non-fatal reinfarction) in the 53 patients with LV hypertrophy and only four events in the remaining 58 patients without LV hypertrophy (RR=2.45; CI=1.76-3.41; P<0.0001). The patients with concentric LV hypertrophy showed a higher incidence of events (64%) than patients with eccentric LV hypertrophy (32%, P<0. 05) and patients with normal geometry and mass (6%, P<0.0001). Multivariate Cox regression model identified concentric geometry as the most powerful predictor of combined end-points (chi(2)=32.7, P<0. 0001). CONCLUSIONS: An increased LV mass and concentric geometry resulted important independent markers of an adverse outcome in patients with a first, uncomplicated myocardial infarction and good LV function.     

A prognostic comparison of asymptomatic left ventricular hypertrophy and unrecognized myocardial infarction: the Framingham Study

In 30 years of follow-up in the Framingham study, routine biennial ECG examinations revealed 315 subjects with ECG-LVH and 164 with unrecognized ECG-MI without previous cardiac explanation. Among subjects initially free of clinically evident coronary heart disease and both ECG abnormalities, the incidence of ECG-LVH was about double that of ECG-MI. Both events exhibited a male predominance and hypertensive subjects were more vulnerable to each. In subjects with asymptomatic ECG-LVH and ECG-MI, the 10-year, age-adjusted incidence of clinical coronary heart disease was greater than the rate experienced by the general Framingham sample. Rates for ECG-LVH were almost as large as those for ECG-MI. Cardiac failure and stroke also occurred more frequently among subjects with either ECG abnormality, and rates for ECG-LVH exceeded those for ECG-MI. Death from coronary heart disease, and sudden death in particular, was also increased two- to fourfold with similar risks for ECG-LVH and ECG-MI. ECG-LVH carried a significantly greater risk than ECG-MI for cardiovascular deaths in women. These findings suggest that ECG-LVH and ECG-MI are similar subclinical events with respect to predisposing characteristics and prognosis for subsequent overt cardiovascular disease including clinical manifestations of coronary heart disease.     

Functional mechanisms of myocardial microcirculation in left ventricular hypertrophy: a hypothetical model of capillary remodeling post myocardial infarction

OBJECTIVES: Left ventricular (LV) remodeling after myocardial infarction (MI) is characterized by myocyte hypertrophy and a disproportional capillary growth. We developed a hypothetical model of capillary remodeling mechanisms based on quantitative data of microcirculation determined by magnetic resonance (MR) imaging techniques and histology. METHODS: Perfusion and regional capillary blood volume (RBV) were quantified 8 and 16 weeks after MI (mean 27.0+/-2.9% of the left ventricle 16 weeks post MI) or sham operation in rats using MR imaging and were correlated with morphometric data. RESULTS: Maximum perfusion (ml/(g min)) in the remote area decreased from 5.69+/-0.63 to 3.48+/-0.48 compared to sham animals (5.33+/-0.31, p相似文献   

心肌梗死后左室重构发病机制进展

急性心肌梗死(AMI)是威胁人类健康的重大疾病,心肌梗死(MI)后30 min,部分心肌细胞即发生不可逆的坏死,因此,MI有效救治的时间窗极为短暂,许多患者不能够得到及时有效的治疗,使得MI后心力衰竭(HF)的发生率仍然居高不下。最新调查研究表明,MI后1年HF的发生率约为14.2%。因MI后HF再次入院的患者,1年死亡率高达为45.5%。MI后HF的主要原因是部分心肌细胞坏死,左室重构,心脏扩张,继而引发HF。目前,MI后左室重构的机制尚未完全阐明。本文介绍了AMI后左室重构的发病机制主要进展。