Should the transvalvular gradient in aortic stenosis be measured?

Moscovitz, Howard L.; Gelb, Ira J.

doi:10.1016/s0002-9149(73)80071-2

Cited by 11 publications

(5 citation statements)

References 15 publications

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“…Among these three exceptions, one patient had severe left ostial and left main coronary artery obstruction demonstrable angiographically and probably sustained minor ischemic myocardial damage, although no definitive electrocardiographic evidence of transmural infarction ensued. In the remaining two exceptions severe calcific aortic stenosis was documented, and occult myocardial damage may have resulted from calcific micro-or macroembolization to the coronary arteries caused by catheter impingement on the diseased valve (25). In each of these three patients with elevated MB CPK activity myocardial damage was confirmed by clinical, ECG, and scintigraphic evidence.…”

Section: Discussionmentioning

confidence: 90%

Determination of the origin of elevated plasma cpk after cardiac catheterization

Roberts

Sobel

Ludbrook

1976

Cathet. Cardiovasc. Diagn.

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Episodes of chest pain are not common in patients undergoing cardiac catheterization. The diagnostic implications of this symptom may be complicated by the occasional appearance of electrocardiographic changes mimicking those seen in acute myocardial infarction, and by the frequent elevation of conventionally measured serum enzymes. Exclusion of infarction is particularly important when coronary revascularization is contemplated. Since the MB CPK isoenzyme is relatively specific to myocardium, we assayed CPK isoenzymes in plasma samples from 184 patients undergoing cardiac catheterization to determine whether CPK elevations accompanying catheterization can be distinguished from those associated with myocardial infarction. Samples were obtained every 2 hr for 24 hr, and CPK isoenzymes quantified by a kinetic fluorometric method. Total plasma CPK increased in all patients (mean peak 0.238 +/- 0.042 (SD) IU/ml) but MB CPK remained normal in 181 patients (less than 0.005 IU/ml). In three remaining patients, MB CPK was elevated and myocardial infarction was confirmed by 99mTc (SN) pyrophosphate scan. Twelve patients after catheterization, in whom no intramuscular premedication was given, exhibited only minimal elevation of total plasma CPK. In contrast, 100 control patients with acute myocardial infarction exhibited peak total CPK activity averaging 0.833 +/- 0.037 (SD), and MB CPK was elevated in all cases (0.078 +/- 0.027 (SD) IU/ml). Thus, CPK elevations after catheterization reflect release of enzyme from noncardiac sources rather than from injured myocardium. Furthermore, increased plasma MB CPK activity may be considered a reliable index of myocardial infarction in patients undergoing cardiac catheterization.

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Section: Discussionmentioning

confidence: 90%

Determination of the origin of elevated plasma cpk after cardiac catheterization

Roberts

Sobel

Ludbrook

1976

Cathet. Cardiovasc. Diagn.

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“…Moscovitz and Gelb [6] have recently questioned the significance of the transvalvar gradient in aortic stenosis, as well as the indications for cardiac catheterization in this condition. They note that in older patients, systolic hypertension and an increased rate of pressure rise may mask aortic stenosis.…”

Section: General Considerationsmentioning

confidence: 99%

“…Other data sometimes used in association with the peak difference are the stroke out put and the duration of ventricular ejection [2], Clinical information which assists in the decision includes the presence of angina, congestive failure, weak delayed arterial pulses [3,4], notching of the carotid arterial up stroke, a loud systolic crescendo-decrescendo murmur, reduced intensity of the aortic second sound, and the absence of evidence of aortic regurgita tion. In children the peak ¿IP tends to be poorly correlated with symptoms, electrocardiogram or the diest film [5], Other hydrodynamic factors also participate in the generation of the peak ¿IP [6] and may greatly modify the diagnosis of the severity of aortic valvar stenosis.…”

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confidence: 99%

Factors Affecting the Transvalvar Pressure Difference in a Hydraulic Model of Aortic Stenosis

1976

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Mechanical factors that can modify the peak transvalvar pressure difference (ΔP) in aortic stenosis were evaluated in a model. A latex rubber sac simulated the ventricle. Expansion of the walls of the sac by means of a negative pressure applied to its outer wall introduced a measured volume into the sac and placed the wall materials under tension. The stretched sac was then permitted to contract and to expel its contents through ‘aortic valvar’ orifices of various severities of stenosis, into an aortic standpipe of selected diameters (compliances). Factors that increased the peak ΔP included the strength (thickness) of the ventricular wall, the rate at which it mobilized and applied its tensile force to compress the sac contents, the unstressed volume of the sac, the total volume in the sac at onset of contraction, the severity of the valvar stenosis, the compliance of the aorta, the rate of arterial run-off, and the aortic diastolic pressure. Loss of forward stroke volume due to mitral regurgitation lowered the peak ΔP. Elevations in diastolic arterial pressure also lowered ΔP. All of these mechanical factors should be considered in the analysis of the severity of clinical aortic valvar stenosis and in decisions for medical therapy and surgical correction. The several factors which do not depend directly on the orifice area or on the forward stroke volume vitiate the sole use of the orifice formula in the analysis of the dynamics of aortic stenosis. The application of this approach in related problems is indicated.

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“…The aortic valve gradient is an important measure of the severity of valvular aortic stenosis [1,2]. Along with the cardiac output, it allows calculation of the aortic valve area by the Gorlin formula [3].…”

Section: Introductionmentioning

confidence: 99%

A safe, rapid method of transfemoral retrograde left ventricular catheterization in valvular aortic stenosis

Little¹,

Arciniegas²,

Mantle³

1981

Cathet. Cardiovasc. Diagn.

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We report our experience with the use of a standard left Amplatz coronary catheter and a guidewire to cross the aortic valve in 34 patients being evaluated for valvular aortic stenosis. A number of 2 Amplatz left coronary catheter inserted via the femoral artery was positioned above the noncoronary aortic valve cusp with the tip aligned toward the aortic valve. This catheter allowed a soft-tipped, Teflon-coated guidewire to be guided through the aortic valve orifice. The catheter was then advanced over the guidewire into the left ventricle. This technique was successful within six minutes in 32 of 34 patients (94%). The stenotic aortic valve was crossed in less than two minutes in 15 patients (42%) and in less than four minutes in 31 (91%). The aortic valve was not crossed in two patients. Twenty-one patients (62%) had an aortic valve area of less than 0.75 cm2. There were no complications. We conclude that this technique provides a method for safe, rapid transaortic left ventricular catheterization in patients with aortic stenosis of all degrees of severity.

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Should the transvalvular gradient in aortic stenosis be measured?

Cited by 11 publications

References 15 publications

Determination of the origin of elevated plasma cpk after cardiac catheterization

Determination of the origin of elevated plasma cpk after cardiac catheterization

Factors Affecting the Transvalvar Pressure Difference in a Hydraulic Model of Aortic Stenosis

A safe, rapid method of transfemoral retrograde left ventricular catheterization in valvular aortic stenosis

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