“…27 The long axis was determined in the right anterior oblique projection as the longest chord originating from the aortomitral angle (Fig 1). The short axis was calculated as the geometric mean of the derived short axes in both left and right anterior oblique projections.…”
BACKGROUND
Nonuniformity is a determinant of diastolic function. In patients with hypertrophic cardiomyopathy, hypertrophy, abnormal calcium handling, and regional ischemia can also play a role. This study was designed to assess regional mechanics, asynchrony, and asynergy in patients with hypertrophic cardiomyopathy.
METHODS AND RESULTS
Nine control subjects and 22 patients with hypertrophic cardiomyopathy were studied by biplane left ventriculography and high-fidelity pressure tracings for the assessment of diastolic function by computing the time constant of isovolumic relaxation, peak filling rate, and the constant of passive chamber stiffness. Regional mechanics were evaluated by dividing the left ventricle into six sectors in the right and left anterior oblique projections. Systolic and diastolic asynchrony were assessed from the coefficient of variation of the regional time intervals from end diastole to end systole and to peak filling rate, respectively. Asynergy was evaluated from the coefficient of variation of the regional area reduction. Regional passive elastic properties were estimated by computing the regional constant of chamber stiffness. In patients with hypertrophic cardiomyopathy, isovolumic relaxation was prolonged (time constant of isovolumic relaxation 101 +/- 41 versus 51 +/- 16 milliseconds in control subjects; P < .001) and the constant of chamber stiffness was increased (0.056 +/- 0.038 versus 0.025 +/- 0.010 mL-1; P < .001). Both systolic and diastolic asynchrony as well as asynergy were found. Regional mechanics showed hyperkinesia in the free wall, whereas the septum exhibited normal wall motion and increased constant of chamber stiffness.
CONCLUSIONS
Diastolic function is impaired in hypertrophic cardiomyopathy, and such an impairment is the consequence of nonuniformity and hypertrophy. The regions where the myopathic process is more pronounced show normal wall motion but increased stiffness. The inhomogeneity of regional wall motion with regional hyperkinesia and normokinesia of neighboring regions results in left ventricular asynergy.
“…27 The long axis was determined in the right anterior oblique projection as the longest chord originating from the aortomitral angle (Fig 1). The short axis was calculated as the geometric mean of the derived short axes in both left and right anterior oblique projections.…”
BACKGROUND
Nonuniformity is a determinant of diastolic function. In patients with hypertrophic cardiomyopathy, hypertrophy, abnormal calcium handling, and regional ischemia can also play a role. This study was designed to assess regional mechanics, asynchrony, and asynergy in patients with hypertrophic cardiomyopathy.
METHODS AND RESULTS
Nine control subjects and 22 patients with hypertrophic cardiomyopathy were studied by biplane left ventriculography and high-fidelity pressure tracings for the assessment of diastolic function by computing the time constant of isovolumic relaxation, peak filling rate, and the constant of passive chamber stiffness. Regional mechanics were evaluated by dividing the left ventricle into six sectors in the right and left anterior oblique projections. Systolic and diastolic asynchrony were assessed from the coefficient of variation of the regional time intervals from end diastole to end systole and to peak filling rate, respectively. Asynergy was evaluated from the coefficient of variation of the regional area reduction. Regional passive elastic properties were estimated by computing the regional constant of chamber stiffness. In patients with hypertrophic cardiomyopathy, isovolumic relaxation was prolonged (time constant of isovolumic relaxation 101 +/- 41 versus 51 +/- 16 milliseconds in control subjects; P < .001) and the constant of chamber stiffness was increased (0.056 +/- 0.038 versus 0.025 +/- 0.010 mL-1; P < .001). Both systolic and diastolic asynchrony as well as asynergy were found. Regional mechanics showed hyperkinesia in the free wall, whereas the septum exhibited normal wall motion and increased constant of chamber stiffness.
CONCLUSIONS
Diastolic function is impaired in hypertrophic cardiomyopathy, and such an impairment is the consequence of nonuniformity and hypertrophy. The regions where the myopathic process is more pronounced show normal wall motion but increased stiffness. The inhomogeneity of regional wall motion with regional hyperkinesia and normokinesia of neighboring regions results in left ventricular asynergy.
“…Left ventricular end diastolic volume and left ventricular end systolic volumes (LVESV) and ejection fraction were calculated from the monoplane angiogram in a 30" right anterior oblique projection using the area length method (34). Left ventricular mass was calculated according to the equation of Trenouth et al (39, which was used to quantitate the equatorial end systolic wall thickness.…”
We assessed coronary reserve, by measuring the increase in coronary sinus blood flow (CSBF) after intravenous administration of dipyridamole (0.14 mgl kg/minute for 4 minutes), in 7 patients with primary scleroderma myocardial disease (PSMD) and in 7 control subjects. Coronary reserve was greatly impaired in PSMD: before administration of dipyridamole, CSBF was similar in patients with PSMD (89 f 32 mllminutel 100 gnn, mean f SD) and in controls (100 f 15 mll minutel100 gm); after dipyridamole infusion, CSBF was significantly lower in patients with PSMD (191 k 45 mll minutdl00 gm) than in controls (399 f 58 mllminutel 100 gm) (P < 0.01). Six of the 7 patients with PSMD had angiographically normal epicardial coronary arteries and normal left ventricular function. Decreased coro--~~
“…Length of the akinetic segment (AKS) was calculated in mm. Left ventricular enddiastolic (EDS) and endsystolic volumes (ESV) were calculated using the area length method of Dodge et al (13). From the angiographically determined volumes, stroke volume (SV = EDV -ESV) and ejection fraction (EF = SV/EDV) were derived.…”
In 7 patients, the recently occluded infarct‐related vessel was recanalized by transluminal catheter techniques during acute myocardial infarction (Group A). 4 patients had single‐vessel disease, 2 patients two‐vessels disease and one, involvement of three vessels. Control angiography was performed in 6 patients, 8 days to 7 months later. Changes of coronary artery anatomy and left ventricular function were compared with a group of 9 conventionally treated patients, who were found to have occlusion of the infarct‐related vessel in the acute stage (Group B). Five Group B patients had one‐vessel disease, 3 patients two‐vessel disease and 1 patient, involvement of all three vessels. In the chronic stage, all transluminally recanalized vessels were found to be patent in Group A. There was spontaneous recanalization of the infarct vessel in 4 of 9 Group B patients. In Group A, the length of the akinetic segment (AKS) decreased significantly (p < 0.05) from 145.4±48.5 mm to 73.2 ± 73.4 mm (mean ± SD). Volume parameters did not change significantly. In Group B, length of the AKS did not change significantly, EDVI increased significantly from 81.1 ±19.8 to 106.8±40.6 ml/m2 (p < 0.05); ESVI increased significantly from 41.7 ± 13.7 ml/m2 to 66.8 ± 37.9 ml/m2 (p < 0.01). In the acute stage, length of the AKS and volume parameters did not differ significantly between the two groups. In the chronic stage, AKS was significantly shorter (A: 73.2 ± 63.4 mm; 144.9 ± 59 mm (p < 0.0025)) and EF was significantly higher (A: 54.6 ±11.6%; B: 40.9 ±14.5% (p < 0.05)) in Group A. Peak CPK was lower in Group A (A: 1009 ± 827 U/l; B: 1324 ± 655 U/l), but this difference did not achieve statistical significance. Results of this pilot study suggest that transluminal recanalization in the early phases of acute myocardial infarction might result in limitation of myocardial injury. However, further research will be needed to improve the technique and to test its results.
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