Determinants and prediction of transmural myocardial perfusion.

Hoffman, Julien I.E.

doi:10.1161/01.cir.58.3.381

Cited by 204 publications

(76 citation statements)

References 57 publications

(6 reference statements)

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“…Eight adult mongrel dogs weighing [20][21][22][23][24][25][26][27][28][29][30] kg (mean 26 kg) were anesthetized with sodium pentobarbital (30 mg/kg). Under sterile conditions, a left thoracotomy was performed in the fifth left intercostal space, the left circumflex coronary artery was dissected free near its origin and a hydraulic occluder made from polyvinyl tubing was positioned around it.…”

Section: Methodsmentioning

confidence: 99%

Dissociation between regional myocardial dysfunction and ECG changes during ischemia in the conscious dog.

Battler¹,

Froelicher²,

Gallagher³

et al. 1980

Circulation

147

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SUMMARY The relations between regional ventricular function and regional and surface ECGs were studied in eight conscious dogs during complete and partial coronary obstructions. Wall thickness and local ECGs were measured using an implanted sonomicrometer, and 11 subcutaneous electrodes were implanted in a modified McFee vectorcardiographic array. Complete obstruction of the circumflex coronary artery (using a hydraulic occluder) produced regional hypokinesia after 15 seconds and regional dyskinesia at 1 minute. Significant ECG changes occurred first in the surface vectorcardiogram, ST segments changed at 30 seconds and mean epicardial and endocardial ECG ST segments increased after 1 minute. During mild partial coronary stenosis that produced stable reductions of systolic wall thickening (%AWT) of less than 25% of control, no ST-segment changes occurred in the surface vectorcardiogram during the 10-minute study period, although ST segments increased significantly in the endocardial and epicardial ECG. With moderate coronary stenoses that produced immediate 25-48% reductions of %AWT (average reduction 36 ± 4%), significant mean ST displacements occurred after 2 minutes in the endocardial ECG, after 3 minutes in the epicardial ECG and after 4 minutes in the surface vectorcardiogram. With coronary stenoses that produced more than 50% reduction of %A.WT (average reduction 69 ± 2%), mean endocardial ST-segment changes were noted after 2 minutes, and changes in both the mean epicardial ECG and the surface vectorcardiogram occurred after 3 minutes. Thus, during mild coronary stenosis, regional myocardial dysfunction can occur without surface ECG changes, while during moderate coronary stenosis, it occurs before endocardial ST-segment changes and precedes surface ECG alterations by several minutes. The surface ECG was slightly more sensitive than the local ECG during complete coronary occlusion and less sensitive during partial coronary obstruction. We conclude that regional contractile abnormalities provide a more sensitive indicator of ischemia than electrocardiographic ST-segment changes.REGIONAL VENTRICULAR dysfunction and STsegment displacement on the ECG are valuable indicators of myocardial ischemia. However, STsegment displacement on the body surface ECG is not specific for ischemia,' and both false-negative and false-positive ECG findings during exercise testing for detecting coronary artery disease have been reported.2 In the experimental setting, regional wall function dynamics are highly sensitive to local ischemia both at rest5 and during exercise in the conscious dog;6 in clinical studies, simultaneous recordings of ventricular function using radionuclide angiographic techniques and ECG recordings during exercise have suggested superiority of mechanical over electrical events for the detection of temporary myocardial ischemia.7-9 Nevertheless, the exercise test with ECG recordings is still the most popular and economical screening test for coronary artery disease in man, 4 1' and further understanding of ...

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Section: Methodsmentioning

confidence: 99%

Dissociation between regional myocardial dysfunction and ECG changes during ischemia in the conscious dog.

Battler¹,

Froelicher²,

Gallagher³

et al. 1980

Circulation

147

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“…No ischemic ST changes were seen with treadmill testing when the DPTI:SPTI was 0.6, whereas ischemia on the ECG only appeared with ratios of 0.45 (2). For AR, a critical DPTI:SPTI of 0.6 was proposed in consideration for the greater extravascular component of coronary resistance in the dilated and possibly hypertrophied heart (8,9,26). We found a DPTI:SPTI of 0.7 to predict cardiovascular mortality from PAR after TAVI, and a causal relation to ischemia was suggested by the higher values of peak TnI after TAVI in patients with DPTI: SPTI Յ 0.7.…”

Section: Discussionmentioning

confidence: 99%

“…Such supplydemand ratio can be estimated from the ratio of the diastolic over systolic pressure time integral (DPTI:SPTI), which sensitively reflects the propensity to myocardial ischemia, notably subendocardial ischemia (7,8). Aortic regurgitation is typically associated with a reduced DPTI:SPTI ratio (7,8,9,13,24,26). We have therefore now calculated the DPTI:SPTI ratio following the TAVI procedure and related it to cardiovascular mortality.…”

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confidence: 99%

Hemodynamic assessment of paravalvular aortic regurgitation after TAVI: estimated myocardial supply-demand ratio and cardiovascular mortality

Patsalis

Konorza

Al–Rashid

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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P. Hemodynamic assessment of paravalvular aortic regurgitation after TAVI: estimated myocardial supply-demand ratio and cardiovascular mortality. Am J Physiol Heart Circ Physiol 304: H1023-H1028, 2013. First published January 11, 2013; doi:10.1152/ajpheart.00807.2012.-A relevant (at least moderate) paravalvular regurgitation (PAR) after transcatheter aortic valve implantation (TAVI) is found in up to 20% of cases and associated with increased mortality. The ratio of the diastolic over the systolic pressure time integral (DPTI:SPTI) has been proposed to reflect an estimate of myocardial oxygen supply versus demand and the propensity for myocardial ischemia. We have now evaluated the potential of this ratio to predict PAR-associated cardiovascular mortality after TAVI, retrospectively analyzing data from 167 consecutive TAVI patients. PAR was graded angiographically, and the myocardial supply-demand ratio was estimated from the planimetric integration of the diastolic and systolic pressure-time area (DPTI and SPTI), respectively. PAR was observed in 113 patients (67%) and angiographically graded as mild in 89 (78.8%), moderate in 21 (18.6%) or moderate to severe in 3 (2.7%) cases. The DPTI:SPTI ratio decreased with increasing Sellers grade of PAR (P Ͻ 0.001). A DPTI:SPTI of Յ0.7 predicted cardiovascular mortality (area under the curve ϭ 0.96). Cardiovascular mortality at 30 days and 1 yr was increased in patients with DPTI:SPTI Յ 0.7 over those with DPTI:SPTI Ͼ 0.7 (42 vs. 2% and 63 vs. 3%, respectively; P Ͻ 0.001). In conclusion, DPTI:SPTI provides an excellent cutoff value of Յ0.7 for the prediction of PAR-associated mortality. aortic regurgitation; aortic stenosis; transcatheter aortic valve implantation.THE INCIDENCE OF moderate and severe paravalvular aortic regurgitation (PAR) after transcatheter aortic valve implantation (TAVI) varies from 10 to 20% (4,5,17,(21)(22)(23)27), and moderate-to-severe PAR after TAVI is associated with increased in-hospital mortality and unfavorable long-term outcome (1,11,14,20). PAR severity during TAVI is usually graded qualitatively using angiography. Quantitative evaluation of PAR has been recently proposed by use of the aortic regurgitation (AR) index, which is calculated as the ratio of the gradient between diastolic aortic pressure (DAP) and left ventricular (LV) end-diastolic pressure (LVEDP) to systolic blood pressure (SBP) ϫ 100 or [(DAP-LVEDP)/SBP] ϫ 100 (20) or more simply by use of the pressure difference between DAP and LVEDP (⌬P DAP-LVEDP ) (14). A pathophysiological understanding of PAR and its consequences is a prerequisite for an effective treatment and the improvement of survival.Myocardial ischemia is traditionally viewed as an imbalance of myocardial oxygen supply over demand. Such supplydemand ratio can be estimated from the ratio of the diastolic over systolic pressure time integral (DPTI:SPTI), which sensitively reflects the propensity to myocardial ischemia, notably subendocardial ischemia (7,8). Aortic regurgitation is typically associated with a reduce...

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“…The endocardial-epicardial ratio increased significantly without a change in total myocardial flow. The redistribution of epicardial flow to the endocardium reflects the reduction in wall tension due to the lowered afterload and preload (left atrial pressure) (21). Inasmuch as myocardial external minute work was also reduced, captopril may favorably alter myocardial oxygen balance and reserve.…”

Section: Discussionmentioning

confidence: 99%

Effects of Captopril on the Distribution of Left Ventricular Output with Ventricular Septal Defect

Boucek

Chang

1988

Pediatr Res

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ABSTRACT. The renin-angiotensin system is activated by congestive heart failure associated with a ventricular septal defect (VSD). To determine the effect of angiotensinconverting enzyme inhibition on the hemodynamics with VSD, the dose response curve of captopril was measured in lambs. Furthermore, the effect of captopril on the distribution of systemic output was determined by the radionuclide-labeled microsphere technique. A total of 12 lambs (less than 1 month old) with VSD were instrumented and a minimum of five animals was tested for each data point. Captopril(0.05-10 mg/kg) caused dose-dependent vascular changes. At a dose of 2 mg/kg, maximal hemodynamic effects were observed. The systemic resistance fell by 28 f 9% (mean f SD, p < 0.05, n = 9), whereas pulmonary arteriolar resistance rose by 113 f 34% ( p < 0.05). These vascular changes caused a reduction in the ratio of pulmonary to systemic flow from 3. Microsphere-determined organ blood flow to the heart, kidney, liver, duodenum, and skeletal muscle was preserved after a 5 mg/kg dose of captopril and, in fact, tended to increase, but the changes were not significant. The myocardial endocardia1 to epicardial flow ratio increased from 1.17 2 0.27 to 1.49 f 0.14 (+27%, p < 0.05). The data indicate that captopril caused dose-dependent changes in the distribution of left ventricular output in lambs with VSD, reducing total pulmonary flow while preserving organ blood flow. (Pediatr Res 24: 499-503, 1988) Abbreviations VSD, ventricular septal defect ANF, atrial natriuretic factor such, serves an homeostatic role to preserve renal function (5). However, this renal-renin response may further impair cardiac performance by increasing afterload (1). The increased afterload may also aggravate the pathophysiology of structural defects with a left-to-right shunt (6).However, local autoregulation may maintain blood flow to vital organs, offsetting the generalized vasoconstriction due to angiotensin 11. The role of the increased angiotensin I1 production may then be to maintain arterial pressure in the autoregulatory range and to preserve organ blood flow despite a reduction in cardiac output (5). If that were the case, inhibiting the formation of angiotensin I1 with a converting enzyme inhibitor might actually impair renal function and possibly organ blood flow in general if the arterial pressure fell below the autoregulatory range. To test the hypothesis that the stimulation in the renin-angiotensin system with a structural heart defect is pathologic and adversely affects the hemodynamics, we created a VSD in lambs. We then determined the dose reponse characteristics of captopril, an angiotensin-converting enzyme inhibitor. Both the global hemodynamics and the regional organ blood flow effects of captopril were studied in nonanesthetized, chronically instrumented animals with electromagnetic flow probes and radionuclide-labeled microsphere injections. MATERIALS AND METHODSThe technique used to create the VSD has been previously described (4) and was not significa...

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Determinants and prediction of transmural myocardial perfusion.

Cited by 204 publications

References 57 publications

Dissociation between regional myocardial dysfunction and ECG changes during ischemia in the conscious dog.

Dissociation between regional myocardial dysfunction and ECG changes during ischemia in the conscious dog.

Hemodynamic assessment of paravalvular aortic regurgitation after TAVI: estimated myocardial supply-demand ratio and cardiovascular mortality

Effects of Captopril on the Distribution of Left Ventricular Output with Ventricular Septal Defect

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