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At least 19 recordsLinked to original sources
PubMed2006

Off-pump revascularization for significant left ventricular dysfunction.

Left ventricular dysfunction is a predictor of perioperative morbidity and mortality in on-pump coronary artery bypass grafting. Obligatory global myocardial ischemia and injury induced during crossclamping as well as adverse systemic effects of cardiopulmonary bypass may induce a disproportionately greater overall physiologic insult in patients with poor ventricular function. All patients undergoing nonemergency off-pump coronary artery bypass by a single surgeon during an 18-month period were retrospectively analyzed. Two groups with preoperative ejection fraction classified as poor (10%-35%; n = 31) or normal (55%-80%; n = 60) were compared. The mean ejection fractions were 26% +/- 1% and 63% +/- 1% respectively, p < 0.000001. In those with significant left ventricular dysfunction, there were 2.8 +/- 0.1 grafts per patient, time to extubation was 8.4 +/- 1.2 hours, and discharge was after 4.9 +/- 0.6 days. These results were statistically equivalent to those in the group with normal left ventricular function. There was no intraaortic balloon pump insertion or mortality in either group. This technique provides an effective means of safely revascularizing patients with significant left ventricular dysfunction, and it may provide a valuable alternative approach in patients with ischemic cardiomyopathy.

Aged↗
PubMed1985

[Effect of aortocoronary bypass surgery on left ventricular function and coronary sinus blood flow in patients with severe left ventricular dysfunction].

Left ventricular function and coronary sinus blood flow were evaluated in 7 patients with severe left ventricular dysfunction at rest before and after aortocoronary bypass surgery, and during exercise after surgery. Same evaluations were performed in 8 normal subject (G-C). Cardiac index (CI) at rest (2.09 +/- 0.55 l/min/m2) significantly increased after operation (2.94 +/- 0.59 l/min/m2) (p less than 0.02). There was no difference between CI during exercise after operation (5.94 +/- 1.51 l/min/m2) and that in G-C. Left ventricular end-diastolic pressure (LVEDP) at rest before operation (16 +/- 8 mmHg) was significantly higher than that in G-C (p less than 0.05). This difference disappeared after operation. LVEDP during exercise after operation (25 +/- 10 mmHg) was significantly higher than that in G-C (p less than 0.01). Coronary sinus blood flow (CSF) at rest (73 +/- 15 ml/min) significantly increased after operation (123 +/- 44 ml/min) (p less than 0.02). There was no difference between CSF during exercise after operation (282 +/- 99 ml/min) and that in G-C. These data indicated that the aortocoronary bypass surgery was effective on left ventricular function and coronary sinus blood flow in patients with severe left ventricular dysfunction.

Adult↗
PubMed2004

Echocardiography in left ventricular dysfunction.

Left ventricular (LV) function is an important predictor of cardiac morbidity and mortality. The role of echocardiography in the assessment of LV function is well established and has been expanded over the last few years with the development of new methodologies. Echocardiography can assess LV global and regional function, as well as systolic and diastolic function. It has the ability to measure volumes, including cardiac output, pressures, LV mass, dP/dt. It can also assess regional dysfunction using the wall motion score. However quantitation by standard echo can be limited, due to poor endocardial definition, time-consuming, and reproducibility, lack of accuracy, particularly considering it takes a lot of geometric assumptions. Therefore, new methodologies have been recently developed to increase echo accuracy. These include the introduction of second harmonics, which is becoming a standard in most equipments; the use of contrast echo to improve LV opacification and endocardial border definition; color kinesis, which allows automated segmental motion analysis; tissue Doppler imaging, which can help in the assessment of regional and diastolic function; and more recently the ability to assess strain and strain rate. This last technology has the ability to quantify local myocardial deformation and it has shown to be a potential strong marker of ischemia, as well as a predictor of LV myocardial recovery postrevascularization. In conclusion, echocardiography is widely used to assess LV function. The recent developments of new ultrasound-related technologies have further increased the interest and importance of echocardiography in the assessment of LV function.

Diastole↗
PubMed2002

Nitric oxide production is maintained in exercising swine with chronic left ventricular dysfunction.

Left ventricular (LV) dysfunction caused by myocardial infarction (MI) is accompanied by endothelial dysfunction, most notably a loss of nitric oxide (NO) availability. We tested the hypothesis that endothelial dysfunction contributes to impaired tissue perfusion during increased metabolic demands as produced by exercise, and we determined the contribution of NO to regulation of regional systemic, pulmonary, and coronary vasomotor tone in exercising swine with LV dysfunction produced by a 2- to 3-wk-old MI. LV dysfunction resulted in blunted systemic and coronary vasodilator responses to ATP, whereas the responses to nitroprusside were maintained. Exercise resulted in blunted systemic and pulmonary vasodilator responses in MI that resembled the vasodilator responses in normal (N) swine following blockade of NO synthase with N(omega)-nitro-L-arginine (L-NNA, 20 mg/kg iv). However, L-NNA resulted in similar decreases in systemic (43 +/- 3% in N swine and 49 +/- 4% in MI swine), pulmonary (45 +/- 5% in N swine and 49 +/- 4% in MI swine), and coronary (28 +/- 4% in N and 35 +/- 3% in MI) vascular conductances in N and MI swine under resting conditions; similar effects were observed during treadmill exercise. Selective inhibition of inducible NO synthase with aminoguanidine (20 mg/kg iv) had no effect on vascular tone in MI. These findings indicate that while agonist-induced vasodilation is already blunted early after myocardial infarction, the contribution of endothelial NO synthase-derived NO to regulation of vascular tone under basal conditions and during exercise is maintained.

Adenosine Triphosphate↗
PubMed1999

Comparison of echocardiography and radionuclide angiography as predictors of mortality in patients with left ventricular dysfunction (studies of left ventricular dysfunction).

Left ventricular (LV) systolic dysfunction, as indicated by a reduced LV ejection fraction (EF) is a potent predictor of cardiovascular mortality. Radionuclide angiography accurately and reproducibly assesses LVEF; however, echocardiography is used more frequently in clinical practice. Whether these methods predict similar mortality has not been fully investigated. We performed a retrospective analysis of patients with baseline radionuclide angiographic (RNA; n = 4,330) and echocardiographic (echo; n = 1,376) based EFs < or =0.35 who were enrolled in the Studies Of Left Ventricular Dysfunction (SOLVD) to address this hypothesis. After adjusting for important prognostic variables, the risk of death (RR 1.15; 95% confidence interval 1.01 to 1.30; p = 0.03) and of cardiovascular death (RR 1.15; 95% confidence interval 1.01 to 1.32; p = 0.04) was higher for patients with ECG-based EFs. To compare the 2 techniques across a range of EF values, we divided the cohort into tertiles of EF. The adjusted risk estimates for all-cause and cardiovascular mortality were similar within each tertile. Of note, the mortality difference in patients with echo- versus RNA-based EFs was most prominent in women. Further, patients with echo-based EFs had significantly higher mortality at sites where this technique was less frequently used to assess the EF. Thus, for a given EF < or =0.35, an echo-based value was associated with a higher risk of death compared with the RNA-based method of measurement. These data suggest that EF values determined by echocardiography and radionuclide angiography predict different mortality and this may, in part, be related to technical proficiency as well as patient characteristics.

Adult↗
PubMed2006

Early postoperative tako-tsubo-like left ventricular dysfunction: transient left ventricular apical ballooning syndrome.

We diagnosed transient left ventricular apical wall motion abnormalities after surgery in a patient presenting with a clinical and electrocardiographic picture of acute myocardial infarction in the absence of significant coronary disease. These angiographic, clinical, and electrocardiographic features satisfied the criteria of the recently described tako-tsubo-like left ventricular dysfunction.

Coronary Angiography↗
PubMed1997

Acute left ventricular dysfunction and left ventricular thrombus in a patient with cerebral hemorrhage.

A 66-year-old woman was admitted to the hospital with a cerebral hemorrhage. An echocardiogram showed severe left ventricular hypokinesis and a left ventricular thrombus. An electrocardiogram showed ST segment elevation in the precordial leads. The patient's creatine kinase level was elevated. A follow-up echocardiogram performed 1 month after admission showed normalization of left ventricular wall motion and disappearance of the thrombus. The results of thallium myocardial scintigraphy, coronary arteriography, and left ventriculography performed 1 month after admission were normal, and the patient was discharged without clinical sequelae. The cause of the patient's left ventricular dysfunction was believed to be not myocardial infarction or myocarditis, but a massive adrenergic discharge due to the cerebral hemorrhage.

Aged↗
PubMed2006

Diastolic and systolic right ventricular dysfunction precedes left ventricular dysfunction in patients paced from right ventricular apex.

BACKGROUND: Cardiac dysfunction after right ventricular (RV) apical pacing is well known but its extent, time frame of appearance and individual effect on left ventricular (LV), RV systolic and diastolic parameters has not evaluated in a systematic fashion. METHODS: Patients with symptomatic bradycardia and ACC-AHA Class I indication for permanent pacemaker implantation (PPI) were implanted a single chamber (VVI) pacemaker. They were followed prospectively by echocardiographic examination which was done at baseline, 1 week, 1 month and 6 months after implantation. Parameters observed were chamber dimensions (M-line), chamber volumes, cardiac output (modified Simpson's method), systolic functions (ejection fraction, pre-ejection period, ejection time and ratio) and diastolic functions( isovolumic relaxation time & deceleration time) of left and right heart. RESULTS: Forty eight consecutive patients (mean age 65.6+/-11.8 yrs, 66.7% males, mean EF 61.82+/-10.36%) implanted a VVI pacemaker were enrolled in this study. The first significant change to appear in cardiac function after VVI pacing was in diastolic properties of RV as shown by increase in RV isovolumic relaxation time (IVRT) from 65.89+/-15.93 to 76.58+/-17.00 ms,(p<0.001) at 1week and RV deceleration time (DT) from 133.84+/-38.13 to 153.09+/-31.41 ms, (p=0.02) at 1 month. Increase in RV internal dimension (RVID) from 1.26+/-0.41 to 1.44+/-0.44, (p<0.05) was also noticed at 1 week. The LV diastolic parameters were significantly altered after 1 month with increase in LV-IVRT from 92.36+/-21.47 to 117.24+/-27.21ms, (p<0.001) and increase in LV DT from 147.56+/-31.84 to 189.27+/-28.49ms,(p<0.01). This was followed by LV systolic abnormality which appeared at 6 months with an increase in LVPEP from 100.33+/-14.43 to 118.41+/-21.34ms, (p<0.001) and increase in LVPEP/LVET ratio from 0.34+/-0.46 to 0.44+/-0.10, (p<0.001)]. The reduction in LV EF was manifested at 6 months falling from 61.82+/-10.36% to52.52+/-12.11%, (p<0.05) without any significant change in the resting cardiac output. CONCLUSION: The present study shows that dysfunction of right ventricle is the first abnormality that occurs in VVI paced patients, which manifests by 1 week followed by LV dysfunction which starts appearing by 1 month and the diastolic dysfunctions precede the systolic dysfunction in both ventricles.

Journal Article↗
PubMedDate not supplied

Left ventricular dysfunction in coronary artery disease: comparison between rest-redistribution thallium 201 and resting technetium 99m methoxyisobutyl isonitrile cardiac imaging.

BACKGROUND: We compared rest-redistribution thallium 201 and resting technetium 99m methoxyisobutyl isonitrile (MIBI) cardiac imaging in 29 men with angiographically proven coronary artery disease and regional ventricular dysfunction. Left ventricular ejection fraction at radionuclide angiography was 35% +/- 9%. METHODS AND RESULTS: Regional left ventricular wall motion was assessed on gated 99mTc MIBI images according to a 3-point scale (0 = normal, 1 = hypokinetic, 2 = akinetic or dyskinetic). 201Tl and 99mTc MIBI uptake values were analyzed quantitatively. A total of 435 myocardial segments were classified on the basis of wall motion analysis into three groups: group 1 (normal wall motion; n = 201), group 2 (hypokinetic; n = 132), and group 3 (akinetic or dyskinetic; n = 102). 201Tl and 99mTc MIBI uptake values were significantly higher in groups 1 and 2 compared with group 3 (p < 0.05) and in group 1 compared with group 2 (p < 0.05). When 201Tl and 99mTc MIBI uptake values were directly compared, no significant differences in group 1 and 2 were observed. In group 3, 99mTc MIBI uptake (67% +/- 14%) was significantly lower (p < 0.001) than initial (72% +/- 11%) and delayed 201Tl uptake (73% +/- 12%). CONCLUSION: Thus rest-redistribution 201Tl and resting 99mTc MIBI cardiac imaging reflect the severity of left ventricular dysfunction in coronary artery disease. However, in segments with severely impaired regional ventricular function, 201Tl uptake is significantly higher than 99mTc MIBI uptake.

Adult↗
PubMed1990

Circulatory support in infants with post-cardiopulmonary bypass left ventricular dysfunction using a left ventricular assist device.

Extracorporeal membrane oxygenation has been advocated as the most appropriate mode of circulatory support in the paediatric age group for post-cardiopulmonary bypass ventricular dysfunction. The results in infants who have predominantly left ventricular failure, or who require such support in order to be weaned off bypass, have been disappointing. Three infants with severe left ventricular dysfunction following cardiopulmonary bypass for correction of congenital heart defects have been managed with a left ventricular assist device. Two required this form of circulatory support in order to be weaned from full bypass while in the third infant it was instituted for progressive left ventricular dysfunction postoperatively. All three were less than 10 kg in weight. Left atrial appendage to aortic bypass was effected using a closed loop circuit with a constrained vortex pump (Biomedicus). Duration of support ranged between 40 and 146 h. One infant made a complete recovery and was able to be discharged home 20 days postoperatively. Another made a circulatory recovery such that both mechanical and inotropic support could be discontinued but had sustained massive neurological damage. The third died of progressive left ventricular dysfunction. This experience with a left ventricular assist device demonstrates that it is technically feasible in small infants, and can be performed to good effect in infants with predominant left ventricular dysfunction following cardiac surgery. It may well be more appropriate than extracorporeal membrane oxygenation in this group of patients.

Cardiac Output, Low↗
PubMed1993

Activation of neurohumoral systems in postinfarction left ventricular dysfunction.

OBJECTIVES: This study was conducted to evaluate the degree of neurohumoral activation around the time of hospital discharge after myocardial infarction. BACKGROUND: Because pharmacologic interventions that block the effects of neurohumoral activation improve the prognosis after infarction, we hypothesized that widespread neurohumoral activation persists in some patients until at least the time of hospital discharge and that the determinants of activation vary from one system to another. METHODS: Five hundred nineteen patients in the Survival and Ventricular Enlargement Study (SAVE) had plasma neurohormones measured before randomization at a mean of 12 days after infarction. All patients had left ventricular dysfunction (left ventricular ejection fraction < or = 40%) but no overt heart failure. RESULTS: Although all neurohormones except epinephrine were increased compared with values in age-matched control subjects, plasma norepinephrine (301 +/- 193 vs. 222 +/- 87 pg/ml, p < 0.001), renin activity (3.0 +/- 3.7 vs. 1.2 +/- 1.2 ng/ml per h, p < 0.001), arginine vasopressin (1.9 +/- 6.9 vs. 0.7 +/- 0.3 pg/ml, p < 0.001) and atrial natriuretic peptide (75 +/- 75 vs. 21 +/- 9 pg/ml, p < 0.001) values ranged from normal to very high, indicating a wide spectrum of neurohumoral activation. Activation of one system did not correlate with activation of another. The clinical and laboratory variables most closely associated with neurohumoral activation were Killip class, left ventricular ejection fraction, age and use of diuretic drugs. The association between neurohumoral activation and clinical and laboratory variables varied from one neurohormone to another. CONCLUSIONS: Neurohumoral activation occurs in a significant proportion of patients at the time of hospital discharge after infarction. Which neurohormone is activated and which clinical and laboratory variables determine this activation vary from one neurohormone to another.

Aged↗
PubMed1991

Experimental model of chronic global left ventricular dysfunction secondary to left coronary microembolization.

A model of chronic left ventricular dysfunction characterized by left ventricular dilation, elevated filling pressures and histologic changes has been lacking. In this study the use of coronary microsphere embolization-induced ischemia was explored as a method of producing chronic left ventricular dysfunction. Acute ischemic left ventricular dysfunction was induced in 13 mongrel dogs with 50 microns plastic microspheres until the peak positive first derivative of left ventricular pressure (dP/dt) decreased by 25% and the left ventricular end-diastolic pressure increased to greater than or equal to 12 mm Hg. After 8 weeks of observation, hemodynamic and echocardiographic variables were measured in each dog. Acute left ventricular dysfunction resulted in a dilated left ventricle with systolic dysfunction (area ejection fraction 24 +/- 6% vs. 57 +/- 9% initially, p less than 0.01) and elevated left ventricular filling pressures. Isovolumetric relaxation was prolonged and the peak rapid filling/atrial filling velocity and integral ratios were reduced. Eight weeks after embolization, there was an increased left ventricular size (end-diastolic area 15.1 +/- 2.1 cm2 at 8 weeks vs. 13.5 +/- 1.4 cm2 early after microsphere injection, p less than 0.05), unchanged end-systolic area, improved area ejection fraction and increased left ventricular mass. Left ventricular end-diastolic pressure increased and, despite continued abnormal relaxation, the peak rapid filling/atrial filling velocity and integral ratios increased to above baseline values, demonstrating a "restrictive" pattern. Gross and histologic examination revealed diffuse, patchy scarring associated with perivascular fibrosis. Thus, coronary microsphere embolization resulted in a model of chronic moderate left ventricular systolic dysfunction and abnormal diastolic function characterized by a "restrictive" filling pattern.

Animals↗
PubMed1992

Characteristics of peak aerobic capacity in symptomatic and asymptomatic subjects with left ventricular dysfunction. The Studies of Left Ventricular Dysfunction (SOLVD) Investigators.

Expired gas analysis was used to determine the aerobic exercise performance of subjects with depressed left ventricular (LV) systolic function and congestive heart failure (CHF). To determine whether subjects with no or minimal CHF have better aerobic exercise performance than do those with overt CHF, oxygen consumption (VO2) at anaerobic threshold (AT) and peak exercise was measured in 184 subjects with LV ejection fraction less than or equal to 0.35 who participated in the Studies of Left Ventricular Dysfunction. Subjects were divided into those with overt CHF needing treatment (treatment trial; n = 20) and those who had neither overt CHF nor treatment for CHF (prevention trial; n = 164). Treatment trial subjects had a lower LV ejection fraction (0.25 +/- 0.07) than did prevention trial ones (0.29 +/- 0.05; p = 0.001), but there were no differences in age, gender, body weight, resting heart rate and blood pressure. Treadmill exercise testing was performed after 2 to 3 weeks of placebo (no angiotensin-converting enzyme inhibitor) treatment. Treatment trial subjects exercised for a shorter time (493 +/- 160 seconds) and attained a lower peak VO2 (13 +/- 4 ml/kg/min) and VO2 at AT (11 +/- 4 ml/kg/min) than did prevention trial ones (842 +/- 277 seconds, and 20 +/- 6 and 16 +/- 5 ml/kg/min, respectively). Analysis of covariance showed that the differences in peak VO2 and VO2 at AT were statistically significant between the 2 trials after adjusting for age, gender, LV ejection fraction and New York Heart Association functional class.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2001

Management of asymptomatic left ventricular dysfunction.

Asymptomatic left ventricular dysfunction should be treated as an early stage on the continuum that is chronic heart failure. The author presents the clinical trial data on which current management with angiotensin-converting enzyme inhibitors and beta-blockers is based. Issues surrounding screening are also discussed.

Adrenergic beta-Antagonists↗
PubMed1997

Late survival after valve operation in patients with left ventricular dysfunction.

BACKGROUND: Left ventricular dysfunction is a predictor of hospital mortality after cardiac valve operation. We evaluated late survival in a large cohort of these patients. METHODS: From 1980 to 1993, 257 patients with a preoperative ejection fraction of 0.40 or less underwent aortic (n = 177), mitral (n = 72), or combined (n = 8) valve operation, with or without concomitant coronary artery bypass grafting. RESULTS: Hospital mortality was 12.5%. Follow-up was 98% complete. Logistic regression analysis showed that an ejection fraction of less than 0.30, mitral regurgitation, concomitant coronary artery bypass grafting, emergency operation, and reoperation were independent correlates of hospital mortality (all at p < 0.05). Kaplan-Meier survival curves of the 220 hospital survivors showed a 65% 5-year survival. Multivariate analysis revealed preoperative use of diuretics, male sex, reoperation, age exceeding 60 years, and aortic regurgitation to be independent predictors of poor late outcome (all at p < 0.05). CONCLUSIONS: The liability of left ventricular dysfunction with regard to diminished long-term survival is not completely reversed by valve operation. If operation is not performed before left ventricular dysfunction develops, postoperative medical treatment of these dilated, remodeled ventricles should be considered.

Adolescent↗
PubMed2006

Pretreatment with angiotensin receptor blockade prevents left ventricular dysfunction and blunts left ventricular remodeling associated with acute myocardial infarction.

BACKGROUND: This study was designed to determine the effects of pretreatment with an angiotensin receptor blocker on left ventricular (LV) function and remodeling during acute myocardial infarction (MI). METHODS AND RESULTS: Sprague-Dawley rats were pretreated with candesartan (10 mg x kg(-1) x d(-1)) for 2 weeks and studied at 1, 3, and 6 minutes after MI. Compared with untreated rats, pretreatment with candesartan lowered (P<0.05) LV systolic pressure and the first derivative of LV pressure with respect to time but did not change LV end-diastolic pressure or improve LV regional function. With candesartan pretreatment, LV fractional shortening and ejection fraction increased (P<0.05) by 37% and 28%, and LV chamber dilation was attenuated (P<0.05). At 6 minutes after MI, LV endothelial nitric oxide synthase decreased in the infarcted and noninfarcted wall 47% (P=0.04) and 70% (P=0.002), and constitutive microtubulin increased 260% (P=0.0005) and 111% (P=0.003). Candesartan had no effect on LV tissue endothelial nitric oxide synthase levels but attenuated the increase in constitutive microtubulin by 77% (P=0.004) and 37% (P<0.05). CONCLUSIONS: Pretreatment with candesartan before an acute MI improves global LV function, prevents LV dilation, and blunts the increase in constitutive microtubulin, with minimal effects on LV hemodynamics, regional function, or tissue endothelial nitric oxide synthase. Thus, candesartan given before an MI attenuates LV remodeling and alters the cytoskeleton matrix of the left ventricle.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

Paradoxical contributions of non-compacted and compacted segments to global left ventricular dysfunction in isolated left ventricular noncompaction.

The pathophysiologic mechanisms of left ventricular (LV) dysfunction in isolated ventricular noncompaction (IVNC) remain unclear. Evaluating global and segmental systolic LV function in 65 patients with IVNC, this study found that normal wall motion was more common in noncompacted than in compacted segments. The number of noncompacted segments per patient correlated positively with the LV ejection fraction and negatively with LV end-diastolic volume index. These paradoxical findings support the concept that noncompaction represents a marker of a more generalized (cardio)myopathy rather than the direct pathophysiologic substrate of this still little-understood disease.

Adult↗
PubMed2004

Plasma MMP-9 and MMP-2 following acute myocardial infarction in man: correlation with echocardiographic and neurohumoral parameters of left ventricular dysfunction.

BACKGROUND: Left ventricular dilatation and elevated plasma natriuretic peptide levels predict adverse prognosis and the development of congestive heart failure after myocardial infarction. Altered matrix metalloproteinase (MMP) activity has been implicated in the structural changes associated with development of heart failure after myocardial injury. The aims of this study were to investigate plasma MMP-2, MMP-9, and tissue inhibitor of metalloproteinase (TIMP)-1 concentrations following acute myocardial infarction and their relationships with measures of left ventricular function. METHODS AND RESULTS: Plasma MMP-2, MMP-9, TIMP-1, and N-terminal proBNP (N-BNP) were quantified on 5 consecutive days in 60 patients with acute myocardial infarction (39 anterior). N-BNP was measured on day 3. Echocardiographic assessment of left ventricular wall motion index and volumes was performed during admission and 6 weeks later. Plasma MMP-9 showed peaks on days 1 and 4. MMP-2 levels, similar on each day, were higher after inferior myocardial infarction. Plasma MMP-2 showed strong, inverse correlation with left ventricular volumes during and after admission. Plasma MMP-9 correlated directly with N-BNP (P=.022) and inversely with wall motion index during admission (P=.05). TIMP-1 levels were higher after anterior (1269, 870-1466 ng/mL) compared with inferior (1183, 856-1419 ng/mL, P=.05) acute myocardial infarction and fell from day 1 through 5 (P <.0005). CONCLUSION: Plasma MMP-9 concentration correlates with neurohormonal and echocardiographic measures of left ventricular dysfunction after myocardial infarction. Higher left ventricular volumes are associated with lower plasma MMP-2 concentrations. Circulating MMP concentrations may provide insights into left ventricular remodeling after acute myocardial infarction.

Adult↗