Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prolonged depression of segmental systolic thickening after brief coronary artery occlusion may result principally from events during reperfusion rather than during the ischemic interval. Thus, cellular calcium overload at reperfusion may be a mediator of contractile dysfunction after brief ischemia, and reduction of calcium entry by diltiazem, a calcium channel antagonist, may enhance recovery of systolic thickening after brief periods of ischemia. Thirteen awake unsedated dogs instrumented with hemodynamic catheters, left anterior descending coronary artery occluders and five to six pairs of intramyocardial sonomicrometers underwent two 15 min coronary artery occlusions with 24 h reperfusion. The order of infusion of diltiazem (15 micrograms/kg per min) or saline solution was alternated. Systolic thickening, hemodynamic variables and regional myocardial blood flow were measured serially over 24 h. Despite equally severe ischemic dysfunction during coronary occlusion, diltiazem-treated segments with systolic thinning during ischemia recovered control segmental thickening significantly earlier than saline solution-treated segments (at 30 versus 180 min of reperfusion). Blood pressure was mildly decreased during diltiazem treatment; therefore, a second group of 10 dogs underwent a similar occlusion and reflow period during infusion of nitroprusside to lower mean arterial pressure equivalently. Decreases in blood pressure in this group resulted in some improvement in segmental systolic function; however, this did not reach statistical significance at any time. Regional myocardial blood flows were similar in the saline solution- and diltiazem-treated groups during ischemia and reflow. Thus, it is concluded that 1) diltiazem infusion significantly enhanced recovery of segmental systolic thickening after 15 min of ischemia and 24 h of reperfusion; 2) the enhancement in segmental systolic function could not entirely be attributed to decreased mean arterial pressure; 3) improvement in postischemic segmental ventricular function was seen only in those segments with systolic thinning during ischemia; thus, segments with the most severe ischemic dysfunction benefited most; and 4) there were no important differences in regional myocardial blood flow during ischemia and reperfusion between saline- and diltiazem-treated animals.
J Am Coll Cardiol 1990 Mar 01
PMID:Differential enhancement of postischemic segmental systolic thickening by diltiazem. 230 44

Increased regional left ventricular function frequently occurs in the nonischemic myocardium after acute coronary occlusion. To further define the regional and global effects of this increased remote function in the ischemic left ventricle, 22 dogs were studied with two-dimensional echocardiography before and 1 h after left circumflex coronary artery occlusion. Two groups of dogs were identified with and without compensatory increased regional left ventricular function, defined as regional wall thickening in the nonischemic zone greater than 2 SD above baseline. After coronary occlusion, nonischemic wall thickening was 76 +/- 15% in the hyperfunction group (n = 11) and 45 +/- 14% in the nonhyperfunction group (n = 11) (p less than 0.001). Despite similar left ventricular end-diastolic cavity areas and equivalent degrees of ischemic wall thinning, dogs with increased left ventricular function in the nonischemic myocardium had a smaller extent of circumferential left ventricular dysfunction (136 +/- 33 versus 170 +/- 43 degrees, p less than 0.001) and a higher area ejection fraction (38 +/- 9% versus 27 +/- 6%, p less than 0.001). These functional differences occurred despite similar myocardial areas at risk by autoradiography (41 +/- 6% versus 37 +/- 12%, p = NS). The data suggest that increased left ventricular function in the nonischemic myocardium determines the global functional impact of acute coronary occlusion and, through interaction with adjacent myocardium, modifies the extent of circumferential left ventricular dysfunction.
J Am Coll Cardiol 1990 Jul
PMID:Augmentation of regional function in nonischemic myocardium during coronary occlusion measured with two-dimensional echocardiography. 235 91

To examine the time course of the functional consequences of progressive left ventricular hypertrophy, diastolic left ventricular inflow and wall thinning variables were analyzed in 13 dogs before and 2, 4, 8 and 12 weeks after creation of perinephritic hypertension. Left ventricular echocardiograms were digitized for dimensions, mass and peak rates of wall thinning (-dh/dt/h) and cavity enlargement (dD/dt/D). Doppler recordings of left ventricular inflow were analyzed for peak early (E) and late (A) diastolic inflow velocities, their ratio and atrial filling fraction. At 2 weeks, systolic blood pressure increased from 151 to 233 mm Hg, wall stress from 52 to 80 kdynes/cm2 and posterior wall thickness from 0.68 to 0.84 cm (all p less than 0.05). Left ventricular mass increased from 90 to 115 g over 12 weeks (p less than 0.05). Heart rate, cavity size and systolic shortening were unchanged at all data points. Diastolic abnormalities accompanied the developing hypertrophy and included impairment of early function, as demonstrated by a peak rate of wall thinning, from -13.4 to -8.9 l/s at 2 weeks (p less than 0.05), increased dependence on atrial systolic filling, a decrease in E/A from 1.68 to 1.29 at 4 weeks (p less than 0.05) and an increase in atrial filling fraction from 30% to 43% at 8 weeks (p = NS). Thus, diastolic dysfunction is an early consequence of experimental left ventricular hypertrophy. Different aspects of diastolic impairment are sensitively reflected by echocardiographic Doppler recordings, suggesting that these methods should be useful for the detection of diastolic dysfunction in human patients.
J Am Coll Cardiol 1989 Feb
PMID:Alterations in diastolic function in response to progressive left ventricular hypertrophy. 252 6

To assess the possible role of restoring forces underlying left ventricular wall motion during rapid filling, the time relations between left ventricular dimensions and filling velocity were studied by digitised M-mode and Doppler echocardiography in 23 normal children and 43 patients: 11 with mild and 17 with severe mitral regurgitation, and 15 with left ventricular hypertrophy due to aortic stenosis. In normal children, peak mitral flow velocity characteristically lagged peak rate of dimension increase by 50 +/- 15 msec, and peak rate of posterior wall thinning by 35 +/- 15 msec, (P less than 0.01 for both). Towards the apex, and along the long axis of the ventricle, these phase differences between dimension and flow velocity were not apparent. The characteristic time relations between flow velocity and transverse dimension were also present in patients with left ventricular hypertrophy or mild mitral regurgitation, but when mitral regurgitation was severe they were lost and there was no significant difference in timing between peak flow velocity and peak rate of dimension change (-2 +/- 30 msec) or wall thinning (-4 +/- 25 msec). We conclude that phase differences between left ventricular wall motion and mitral inflow velocity are present in the normal ventricles of children. They cannot be explained on the basis of simple shape changes or passive filling of the relaxing ventricle, but strongly suggest the additional presence of ventricular restoring forces. They persist in patients with left ventricular hypertrophy or mild mitral regurgitation, but are lost when the regurgitation is severe, the filling pattern reverting to that predicted for passive distension of the ventricular cavity by a high left atrial pressure.
Int J Cardiol 1989 Sep
PMID:Phase differences between left ventricular wall motion and transmitral flow in man: evidence for involvement of ventricular restoring forces in normal rapid filling. 252 30

Evidence of acute infarct expansion and the frequency of the acute infarct expansion syndrome (acute infarct dilatation and thinning associated with hypotension and left ventricular failure but no evidence of new necrosis) occurring at two days or more after a first acute Q-wave myocardial infarction were studied using serial two-dimensional echocardiography in 221 consecutive patients (100 anterior, 121 inferior). Patients with symptomatic pericarditis were treated with indomethacin (group 1, n = 73) or ibuprofen (group 2, n = 49) and those without symptomatic pericarditis received neither drug (group 3, n = 99). The overall frequency of the acute infarct expansion syndrome was 13% and 69% of these were among the pericarditis groups. The syndrome was significantly more frequent in group 1 (22%) than group 2 (8%) (P less than 0.05) or group 3 (9%) (P less than 0.025). Serial echocardiograms revealed more expansion with greater percentage increase in the infarct containing segment length in group 1 than group 2 or group 3 (18% versus 9% versus 9%, P less than 0.005). However, the decreases in infarct segment thickness were similar in groups 1 (24%) and 2 (25%) but greater (P less than 0.001) than in group 3 (7%). Despite similar infarct size and infarct thinning in groups 1 and 2, the degree of infarct expansion was greater and the infarct expansion syndrome more frequent in group 1. However, when allowance was made for the potential protective effect of prior use of intravenous nitroglycerin and concomitant use of nifedipine, indomethacin and ibuprofen had similar effects on expansion. Thus, indomethacin or ibuprofen should be used with caution after Q-wave infarction so as to avoid further expansion. The fact that short term use of other drugs might modify infarct remodelling should be considered in studies attempting to assess efficacy of one particular drug.(ABSTRACT TRUNCATED AT 400 WORDS)
Can J Cardiol 1989 May
PMID:Myocardial infarct expansion during indomethacin or ibuprofen therapy for symptomatic post infarction pericarditis. Influence of other pharmacologic agents during early remodelling. 256 3

The influence of changes in preload, afterload and contractile state on left ventricular (LV) filling characteristics were examined. Normal subjects underwent echocardiographic determination of the peak rates of LV dimension change and wall thinning and their respective timing at rest, after preload augmentation with dextran, during increased afterload with methoxamine and during inotropic stimulation by dobutamine. These 2 peak velocities and their timing in diastole correlated well with each other and responded similarly to interventions. Increased preload resulted in higher peak velocities of dimension change and wall thinning, without changing the time in diastole at which they occur. Both peak velocities moved later into diastole with higher afterload; however, the overall change in magnitude was variable and without statistical significance. Inotropic stimulation resulted in faster rates of peak dimension change and wall thinning, which occurred at an earlier point in diastole. Examination of various measures of LV size and function over a wide range of preload and afterload conditions under a constant contractile state revealed a complex set of relations. The ratio of wall thickness-to-dimension at end-diastole showed the most significant relation to the peak rate of dimension change, whereas peak thinning was best correlated with fractional wall thickening. Both velocities were also significantly but more weakly related to other variables of systolic function. The timing of these peak velocities correlated most closely with the end-systolic wall stress and heart rate. Thus, LV filling and wall thinning depend in a complex fashion on loading conditions, heart rate and contractile state.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1985 Mar 01
PMID:Effects of loading conditions and contractile state (methoxamine and dobutamine) on left ventricular early diastolic function in normal subjects. 257 37

Recent studies suggest that neutrophil accumulation and activation in postischemic myocardium may be responsible for myocardial no reflow, which is characterized by an incomplete restoration of blood flow after reperfusion. To examine this further, 11 open chest, anesthetized dogs received bolus injections of a bovine neutrophil antiserum that produced an average 81 +/- 5% depletion of circulating neutrophils, and 10 control dogs received nonimmune serum. Each animal underwent 2 h of left circumflex artery occlusion followed by 4 h of reperfusion. Simultaneous two-dimensional echocardiography and radioactive microsphere blood flow studies were performed at baseline, 2 h of occlusion and early (approximately 5 min) and 4 h of reperfusion. During occlusion, both groups developed similar reductions in myocardial blood flow and levels of ischemic zone myocardial wall thinning. At early reperfusion, similar levels of hyperemia and regional hypokinesia were observed for both groups. By late reperfusion, both groups experienced significant no reflow in the subendocardium (p less than 0.05) and reduced reflow in the mid-myocardium. Regional depression in ischemic zone function persisted throughout the reperfusion period in both groups. However, infarct size expressed as a percent of left ventricular weight, assessed by triphenyltetrazolium chloride staining, was smaller for the neutrophil depletion group compared with the control group (8.7 +/- 1.3% versus 13.1 +/- 1.8%, p less than 0.05). It is concluded that an 81% neutrophil depletion fails to modify the no reflow phenomenon or improve functional recovery after 2 h of coronary artery occlusion and 4 h of coronary reperfusion despite modification of the ultimate size of necrosis.
J Am Coll Cardiol 1989 Dec
PMID:Neutrophil depletion fails to modify myocardial no reflow and functional recovery after coronary reperfusion. 258 73

This study describes the long-term outcome of 33 patients with hypertrophic cardiomyopathy who experienced a cardiac arrest but were successfully resuscitated. Cardiac arrest occurred at ages 9 to 62 years (mean 32); five patients survived multiple (two or three) arrests. A variety of treatments were administered; 18 patients with left ventricular outflow tract obstruction underwent ventricular septal myotomy-myectomy or mitral valve replacement and also received drug therapy; 15 patients received medical therapy alone. To date, 22 (67%) of the 33 patients have survived after the initial cardiac arrest for periods of 17 months to 22 years (mean 7 years); 12 patients have survived for greater than or equal to 5 and 6 for greater than or equal to 10 years. Of the 22 survivors, 16 have remained asymptomatic or only mildly symptomatic over the period of follow-up; 6 others have become severely symptomatic with heart failure, including 3 with evidence of left ventricular wall thinning and cavity enlargement. Eight patients ultimately died of natural cardiac causes (suddenly or of progressive heart failure) 7 months to 8.4 years (mean 4 years) after their initial cardiac arrest. Actuarial patient survival was 97 +/- 3%, 74 +/- 9% and 61 +/- 11% after 1, 5 and 10 years, respectively. Event-free rate (defined as actuarial survival without recurrent cardiac arrest of death) was 83 +/- 7%, 65 +/- 9% and 53 +/- 11%, respectively. For this group of patients with hypertrophic cardiomyopathy who were treated in a nonsystematic fashion with a variety of therapeutic strategies, the long-term outcome after surviving a cardiac arrest was variable.(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1989 May
PMID:Long-term outcome of patients with hypertrophic cardiomyopathy successfully resuscitated after cardiac arrest. 270 10

Noninvasive measurement of myocardial blood flow in absolute terms (i.e., milliliters per gram per min) has been difficult to accomplish despite the intrinsically quantitative power of positron emission tomography because of the nonphysiologic nature of tracers that have been employed conventionally as well as the limited spatial resolution of currently available instruments. It was previously demonstrated that myocardial blood flow in animals can be quantitated accurately with the diffusible tracer oxygen-15-labeled water (H2(15)O) when the arterial input function and myocardial radiotracer concentration were measured directly. To extend the approach for completely noninvasive measurement of blood flow, a parameter estimation procedure was developed whereby effects of limited tomographic spatial resolution and cardiac motion were compensated for within the operational flow model. In validation studies in 18 dogs, myocardial blood flow measured with positron emission tomography after intravenously administered H2(15)O correlated closely with flow measured with concomitantly administered radiolabeled microspheres over the range of 0.29 to 5.04 ml/g per min (r = 0.95). Although regional ischemia was clearly identifiable tomographically, absolute flow could not be determined accurately in ischemic regions in four dogs because of poor count statistics related to wall thinning. Subsequently, myocardial blood flow was measured in 11 normal human subjects. Flow was homogeneous throughout the myocardium, averaged 0.90 +/- 0.22 ml/g per min at rest and increased to 3.55 +/- 1.15 ml/g per min after intravenous administration of dipyridamole. Therefore, positron emission tomography with H2 15O and the approach developed permits noninvasive measurement of myocardial blood flow in absolute terms in humans and should facilitate objective assessment of interventions designed to enhance nutritive perfusion.
J Am Coll Cardiol 1989 Sep
PMID:Noninvasive quantitation of myocardial blood flow in human subjects with oxygen-15-labeled water and positron emission tomography. 278 69

Myocardial reperfusion after reversible ischemia is known to be associated with prolonged abnormalities of systolic contractile function (myocardial "stunning"). However, no information is available regarding the recovery of diastolic function in the stunned myocardium in the conscious state. Accordingly, 10 conscious dogs instrumented with pulsed Doppler thickening probes underwent a 15 min occlusion of the left anterior descending coronary artery followed by 7 days of reperfusion. Regional systolic function was assessed as net systolic thickening fraction. Left ventricular regional diastolic properties were estimated from two variables: the mean rate to half end-diastolic thinning and the late diastolic thinning fraction. Both indexes of diastolic function remained severely impaired after restoration of flow. In general, the recovery of the mean rate to half end-diastolic thinning and of the late diastolic thinning fraction paralleled the recovery of systolic thickening, but the impairment of the mean rate to half end-diastolic thinning was more marked than that of the late diastolic thinning fraction. At 4 h of reperfusion, the values for the mean rate to half end-diastolic thinning and the late diastolic thinning fraction (expressed as percent of baseline) were 57 +/- 5% (p less than 0.001 versus baseline) and 79 +/- 7% (p less than 0.05), respectively, whereas systolic thickening fraction averaged 52 +/- 10% (p less than 0.001). At 24 h, the mean rate to half end-diastolic thinning and the late diastolic thinning fraction were no longer significantly different from baseline, whereas systolic thickening fraction remained decreased at 82 +/- 4% (p less than 0.001) and returned to control values by 48 h. This study demonstrates the presence of profound, prolonged abnormalities of regional diastolic wall thinning after a brief episode of ischemia in the conscious state and expands the concept of myocardial stunning from the traditional notion of impaired systolic performance to that of a global derangement in mechanical function that involves both systolic and diastolic properties.
J Am Coll Cardiol 1989 Jan
PMID:Prolonged abnormalities of left ventricular diastolic wall thinning in the "stunned" myocardium in conscious dogs: time course and relation to systolic function. 290 66


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>