Hemodynamics of valvular disorders as measured by cardiac catheterization

INTRODUCTION — Pressure waveforms obtained during cardiac catheterization can be used to diagnose and evaluate congenital or acquired valvular heart disease [1-3]. However, echocardiography provides adequate diagnostic data in most patients.

In a minority of patients with valvular heart disease (<5 percent), further evaluation with invasive intracardiac pressure measurements and/or angiography is needed because the echocardiographic data are nondiagnostic or there is a discrepancy between the clinical presentation and echocardiographic findings. Invasive hemodynamic measurements are also used to monitor therapeutic percutaneous procedures such as transcatheter aortic valve replacement, transcatheter mitral valve repair with a clip, and balloon valvotomy.

Coronary angiography is often needed before transcatheter valve implantation or surgery, but hemodynamic measurements are not recommended if noninvasive data are diagnostic.

An overview of the hemodynamics of stenotic and regurgitant valvular lesions, as measured by cardiac catheterization, will be provided here. The clinical characteristics of valvular heart disease are discussed separately.

AORTIC STENOSIS — Regardless of etiology, stenosis of the aortic valve causes obstruction of blood flow from the left ventricle (LV) to the aorta. As a result, there is a systolic pressure gradient across the valve with a higher pressure in the LV than the aorta [4]. As discussed separately, valvular aortic stenosis (AS) should be distinguished from subvalvular and supravalvular AS. (See "Clinical manifestations and diagnosis of aortic stenosis in adults".)

Echocardiography has largely supplanted cardiac catheterization in the evaluation and monitoring of patients with AS (table 1). The 2020 American College of Cardiology/American Heart Association (ACC/AHA) guidelines recommended cardiac catheterization for assessment of AS if noninvasive data are nondiagnostic or if there is a discrepancy between clinical and echocardiographic evaluation [2]. (See "Clinical manifestations and diagnosis of aortic stenosis in adults".)

There is a rare risk of cerebral embolization associated with crossing the aortic valve in patients with severe calcific AS; as a result, this approach should be avoided if not required [5,6]. The risk appears to be higher than in other patients undergoing cardiac catheterization. (See "Stroke after cardiac catheterization", section on 'Incidence'.)

The separate issue of coronary angiography before aortic valve replacement to identify patients who might also benefit from coronary artery bypass graft surgery is discussed elsewhere. (See "Indications for valve replacement for high gradient aortic stenosis in adults", section on 'Concomitant coronary revascularization'.)

Aortic valve gradient is best measured by one of several methods to measure simultaneous LV and aortic pressure (from least to most accurate):

●Single-catheter LV-aortic pullback (not accurate enough)

●LV catheter through arterial sheath (longer sheath better than shorter)

●Bilateral arterial access (2 catheters)

●Double-lumen pigtail catheter (no longer available)

●Double-lumen PA balloon tipped catheter (rarely used)

●Mother-and-child aortic guide catheter with smaller pigtail to LV

●Transeptal (venous access) catheter to LV with central aortic pressure (arterial access)

●Diagnosis catheter in aorta with 0.014" pressure guidewire in LV.  (Micro pressure catheter work too)

●Multi-transducer micromanometer catheters (pricey and not disposable)

●Dual sensor pressure guidewire (in development)

Aortic valve gradient — A precise assessment of the aortic valve gradient can be obtained by the simultaneous measurement of the aortic and LV pressure assessed with a dual lumen pigtail catheter measuring pressure above and below the aortic valve within the LV. For research purposes, dual high fidelity transducer catheters are also available (figure 1). Historically, the aortic pressure was estimated from peripheral arterial pressure, realignment of the pressure tracing is necessary since the peripheral arterial pressure is delayed by wave transmission to the extremity compared with the central aortic pressure (waveform 1 and waveform 2). (See "Aortic valve area in aortic stenosis in adults".)

Although the most common qualitative assessment of a transvalvular gradient in clinical practice is the observation of pressure during LV catheter pull back from the LV to a level just above the aortic valve, it is not useful for quantitative calculations.

The time-honored method of evaluating the severity of AS is a calculation of aortic valve area (AVA in cm²) based upon the formulations described by Gorlin and Gorlin [7]:

where SV = stroke volume (mL per beat), SEP = systolic ejection period (seconds per beat), and ΔP = mean systolic pressure gradient between the LV and aorta (mmHg). (See "Aortic valve area in aortic stenosis in adults", section on 'Gorlin equation for aortic valve area'.)

Alternatively, the Hakki formula is nearly equivalent to the simplified Gorlin formula:

where CO = cardiac output (mL/min), LV = left ventricular systolic pressure (mmHg) and Ao is aortic systolic pressure (mmHg). Accuracy may be diminished in bradycardia (heart rate <60 beats per minute) and tachycardia (heart rate >100 beats per minute).

Aortic pressure — A reduced aortic pressure with delayed rise in the pressure upstroke, loss of the dichrotic notch, and the existence of a pressure gradient between the LV and the aorta are the principal findings related to the aortic pressure among patients with aortic valvular stenosis (figure 1). The rise in aortic pressure is slow and delayed compared with the pressure rise in the LV. Loss of the dichrotic notch (ie, calcific valve without distinct closure) is associated with a single S2 a marker of severe AS.

Left ventricular pressure — In addition to an increased systolic pressure, abnormalities of diastolic pressure may be observed because of LV hypertrophy with reduced compliance. Although the mean LV diastolic pressure may be normal or elevated, the LV end-diastolic pressure is commonly elevated, a result of filling of the noncompliant LV after atrial systole. Thus, there is usually a prominent "a" wave with increased amplitude (figure 2 and figure 3).

Left atrial or pulmonary capillary wedge pressure — The left atrial pressure tracing shows large "a" waves because of the combination of a hypertrophied left atrium and a stiff or noncompliant LV; this reflects the increased pressure generated during atrial contraction and filling of the LV.

Low-gradient aortic stenosis — An important group of patients with AS consists of symptomatic patients who have low-gradient AS, defined as a small transvalvular gradient (<30 mmHg), and a low cardiac output, with a calculated aortic valve area of ≤0.7 cm² [8]. In these patients, there is often doubt about whether the aortic valve is sufficiently stenotic to account for the symptoms or the patient has only mild aortic valvular disease and the symptoms are resulting from a significant reduction in LV function due to a myopathic problem. (See "Clinical manifestations and diagnosis of low gradient severe aortic stenosis".)

The concern about low-gradient AS is justified, since the Gorlin formula is flow-dependent and tends to underestimate the valve area when the cardiac output is low, ie, <3 L/min [9,10]. Since cardiac output measured at the time of cardiac catheterization greatly influences the clinical evaluation and subsequent management decisions, the use of valvular resistance, which is a useful adjunct to the Gorlin formula in this clinical situation, and recalculation of the aortic valve area after a pharmacologic stimulation of cardiac output (such as with dobutamine) are often required for further evaluation to facilitate the decision regarding surgery in these patients. Maneuvers that increase cardiac output will increase calculated valve area, except in truly severe AS. The 2020 ACC/AHA guidelines for valvular heart disease note that in patients with suspected low-flow, low-gradient severe AS with reduced LVEF (stage D2), low-dose dobutamine stress testing with echocardiographic or invasive hemodynamic measurements is reasonable to further define severity and assess contractile reserve [2]. (See "Clinical manifestations and diagnosis of low gradient severe aortic stenosis".)

Distinguishing aortic stenosis from hypertrophic cardiomyopathy — Certain characteristics of the pressure gradient help distinguish hypertrophic cardiomyopathy (HCM) from aortic valvular disease. As examples, the obstruction in HCM, unlike that due to aortic valvular disease, is associated with the following features:

●The pressure gradient is within the LV (intraventricular) (waveform 3).

●The pressure gradient may be variable and labile. When the LV outflow tract gradient is obstructive, the aortic pressure has a characteristic "spike and dome" configuration of early LV obstruction.

●The timing and upstroke of the initial LV and the aortic pressure tracings are similar and rapid in upstroke (as compared with slow upstroke in AS).

●A premature ventricular contraction can distinguish AS from HCM. In HCM, postextrasystolic potentiation produces an increase in LV contractility, which may result in an increase in SAM and outflow obstruction, and a decreased aortic pulse pressure (Brockenbrough-Braunwald-Morrow sign).

The hemodynamics of hypertrophic cardiomyopathy are discussed separately. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation".)

CHRONIC AORTIC REGURGITATION — Due to inadequate valvular closure, aortic regurgitation results in the backward flow of blood from the aorta to the LV during diastole. This may be due to a primary abnormality of the valve leaflets, the wall of the aortic root, or both. (See "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults".)

Despite the absence of a fixed stenotic lesion in most patients with aortic regurgitation, the large stroke volume crossing the aortic valve (which has a fairly fixed diameter) may infrequently result in a small systolic gradient, which reflects "relative" stenosis due to high flow during LV ejection.

In aortic regurgitation, the LV stroke volume (A) (measured angiographically) is greater than the forward stroke volume (F) (determined by the Fick cardiac output); the difference is the regurgitant fraction (RF) that leaks back into the LV during each cardiac cycle.

The 2020 American College of Cardiology/American Heart Association guidelines recommended cardiac catheterization in patients with aortic regurgitation when noninvasive tests are inconclusive or provide discrepant results from clinical findings [2]. Cardiac catheterization should be performed with aortic root angiography and measurement of LV pressure to assess the severity of the regurgitation, aortic root size, and LV function.

Aortic pressure — The aortic pressure tracing in aortic regurgitation reveals a rapid upstroke (due to augmented LV contractility) and an increased systolic pressure (due to increased stroke volume). However, a rapid fall in the aortic pressure results from the regurgitation. At the end of diastole, near equalization of the aortic and LV pressures occurs because of the continuous leaking of blood back into the LV producing a rapid rise in LV pressure across diastole. The pulse pressure, which is defined as the systolic minus the diastolic pressure, is therefore widened, since the systolic and diastolic pressures are raised and reduced, respectively (figure 4).

Left ventricular pressure — The LV end-diastolic volume is increased; however, the LV end-diastolic pressure is usually normal or only slightly elevated since LV compliance is also increased as the LV compensates (figure 4). The LV systolic pressure may be normal or elevated, because of the increased diastolic volume and augmented LV contractility.

Left atrial pressure — With isolated aortic regurgitation, the left atrial pressures and waveform are usually normal. However, if LV hypertrophy is present, there may be a somewhat increased "a" wave, like that observed in AS.

ACUTE AORTIC REGURGITATION — With acute aortic regurgitation, the usual adaptation of the LV to chronically large regurgitant volumes (eg, enhanced compliance) has not had time to develop. As a result, the increased diastolic volume in the LV leads to a marked elevation in LV pressures. (See "Acute aortic regurgitation in adults".)

The LV pressure tracing reveals a steep rise in diastolic pressure and a markedly elevated LV end-diastolic pressure (which is equivalent to the aortic end-diastolic pressure). Since forward stroke volume declines, aortic systolic pressure is reduced and the pulse pressure is therefore smaller. In addition, the left atrial pressure is elevated. The pressure tracing shows a small "a" and "v" wave, and the nadir of the "x" and "y" descents are less than normal.

CHRONIC MITRAL REGURGITATION — Regurgitation of the mitral valve produces a backflow of blood from the left ventricle (LV) to the left atrium during systole. This disorder may be due to abnormalities of the mitral valve leaflets, chordae tendineae, papillary muscles, or annulus (figure 5), all of which result in inadequate closure (also known as coaptation) of the two mitral leaflets. (See "Clinical manifestations and diagnosis of chronic mitral regurgitation".)

The regurgitant flow produces a large left atrial pressure wave immediately with the onset of ventricular systole (waveform 4). During the initial part of diastole, the left atrium rapidly decompresses with a large antegrade flow to the LV.

In mitral regurgitation, the LV stroke volume (A) (measured angiographically) is greater than the forward stroke volume (F) (determined by the Fick cardiac output); the difference is the regurgitant fraction (RF) that leaks back into the left atrium during each cardiac cycle:

Left atrial pressure — With chronic mitral regurgitation, the direct transseptal measurement of the left atrial pressure demonstrates a marked pressure increase with the very onset of systole, thereby producing a tall "v" wave. Since the "c" wave may not be apparent, this has also been termed a "c-v" wave (waveform 4 and waveform 5).

The height of the 'v' wave is a sensitive but not a specific marker for mitral regurgitation; these waves are frequently associated with a ventricular septal defect and with disorders associated with altered compliance and pressure-volume relationships within the atrial and ventricular chambers.

With chronic mitral regurgitation, the LV and left atrium directly communicate during systole. However, despite the large volume of blood in the left atrium, the mean left atrial pressure may be normal or only slightly increased; this is largely due to a very compliant left atrium, which dilates in response to the volume overload.

The amplitude of the tall "v" wave is therefore less than that of LV systole. By comparison, the amplitude of the "a" wave is often reduced because of left atrial distension and dysfunction. Left atrial pressure in diastole is normal and is similar to the LV diastolic pressure (waveform 5).

The pressure-volume curve produces different "v" waves depending upon volume and left atrial compliance (figure 6). With a left atrium of low compliance, increasing pressure is obtained with increasing flow or volume in the left atrium; in this setting, a large "v" wave can be associated with a small increase in pressure. By comparison, a higher compliance of the left atrium would yield a much smaller "v" wave. The administration of vasodilators frequently shifts the pressure-volume curve to a lower level.

Left ventricular pressure — In chronic mitral regurgitation, the LV is volume overloaded due to the excess blood volume (generated during the prior systolic regurgitant beat) flowing during diastole from the left atrium. However, since the compliancy of the LV increases, the LV systolic and diastolic pressures are normal or only slightly increased. Although the LV stroke volume is increased, the forward stroke volume is normal because a part of the stroke volume regurgitates back into the left atrium. The LV pressure waveforms in systole and diastole are therefore normal.

An assessment of the severity of mitral regurgitation uses the ratio of the area under the V wave to the LV systolic area (Va/LVa) obtained during transseptal catheterization. In this first report of this methodology, the Va/Lva was significantly lower in patients with 0-1+ MR compared with =2+ MR (0.14 versus 0.23) [11].

ACUTE MITRAL REGURGITATION — With acute mitral regurgitation, the left ventricle (LV) and (more importantly) the left atrium have not had time to adapt to the regurgitant volume overload, resulting in low compliance chambers. As a result, with the onset of systole and the large volume of regurgitant blood flow, the left atrial pressure rises abruptly, causing a very tall "v" wave. Because of this "v" wave, the pressure gradient between the left atrium and LV declines by the end of systole; the amplitude of the "v" wave and that of LV systole are nearly equivalent. The diastolic pressure of the LV is increased because of an increase in the end-diastolic volume within an undilated and noncompliant chamber.

MITRAL STENOSIS — In pure mitral stenosis (MS), there is impairment of blood flow from the left atrium into the left ventricle (LV), resulting in a pressure gradient between the two chambers during diastole. (See "Rheumatic mitral stenosis: Clinical manifestations and diagnosis".)

The 2020 American College of Cardiology/American Heart Association (ACC/AHA) valve guidelines note that adequate assessment of MS is generally obtained by transthoracic echocardiography, occasionally supplemented by transesophageal echocardiography [2]. Cardiac catheterization is indicated when noninvasive evaluation is nondiagnostic or if clinical and echocardiographic findings are discordant. The 2020 ACC/AHA guidelines for valvular heart disease note that in patients with rheumatic MS and a discrepancy between resting echocardiographic findings and clinical symptoms, exercise testing with Doppler or invasive hemodynamic assessment is recommended to evaluate symptomatic response, exercise capacity, and the response of the mean mitral gradient and pulmonary artery pressure [2].

Mitral valve gradient — In the cardiac catheterization laboratory, the severity of MS as reflected by the mean mitral valve gradient (MVG) is measured during diastole by the simultaneous comparison of the LV pressure (obtained with an LV catheter positioned retrogradely from the aorta), and the left atrial pressure (measured directly using a transseptal catheter or indirectly with a pulmonary artery catheter in the wedged position [PCWP]) (waveform 6). The MVG is the difference between the mean left atrial pressure (MLAP) and the mean LV pressure (MLVP) during diastole. In most cases a gradient is present, although it decreases during diastole because of slow but continuous left atrial emptying. With atrial systole, however, the gradient increases and is markedly higher than the LV end-diastolic pressure.

Since the diastolic filling period is important in the assessment of mitral valve gradients, the heart rate's effect upon the mitral valve gradient is important. The gradient is higher with a faster heart rate since less time is available for left atrial emptying with a reduced diastolic period. By comparison, the gradient is lower with a slower heart rate.

Among patients in atrial fibrillation, the severity of MS as assessed via the PCWP may differ from that obtained with the direct measurement of left atrial pressure. Patients who are in atrial fibrillation require planimetry and the average of valve gradients over at least 10 cardiac cycles (figure 7)[3]. These factors are evident at cardiac catheterization and should be considered in the computation of mitral valve stenosis [12].

A simplified method for estimating the mean mitral valve gradient (MVG) has been developed in which mean LV diastolic pressure is estimated as LVEDP/2 [13], thus:

One potential limitation of this simplified method is that tachycardia may reduce the accuracy of the LV diastolic pressure estimate with resultant overestimation of valve stenosis severity. One advantage of the simplified method is that it does not require simultaneous recording of LV and left atrial diastolic pressures.

The time-honored method of evaluating the severity of MS is a calculation of mitral valve area (MVA in cm²) based upon the formulations described by Gorlin and Gorlin [7]:

where SV = stroke volume (mL per beat), DFP = diastolic filling period (sec per beat), and ΔP = mean diastolic pressure gradient between the left atrium and LV (mmHg). The Gorlin formula is best applied to patients in sinus rhythm without mitral regurgitation, normal LV function, and no other concomitant valve lesions.

Left atrial pressure — As a result of the impairment to blood flow during diastole, the volume of blood in the left atrium and the mean left atrial pressure are both increased during this period. After mitral valve opening, the pressure only gradually decreases and the "y" descent is gradual. The "a" wave, which is due to left atrial contraction, is markedly increased because of the stenosis (waveform 6).

Left ventricular pressure — Since the valve abnormality is proximal to the LV, the pressure waveforms are normal except for a reduced amplitude of the "a" wave. The LV end-diastolic pressure may be lower than normal because of the impaired filling of the LV from the left atrium.

TRICUSPID REGURGITATION — Tricuspid regurgitation produces a backflow of blood from the right ventricle to the right atrium during systole. Inadequate closure of the three tricuspid leaflets results because of abnormalities of the tricuspid valve leaflets, chordae tendineae, papillary muscles, or annulus (see "Etiology, clinical features, and evaluation of tricuspid regurgitation"). It may also occur with certain arrhythmias.

Tricuspid regurgitant flow produces a distinct right atrial pressure waveform with the transmission of the regurgitant wave into the right atrium, the vena cava, and ultimately the jugular veins (figure 8) [14-16]. The manifestations of tricuspid regurgitant flow are therefore evident by inspection of the neck veins.

Right atrial pressure — The right atrial pressure waveform with tricuspid regurgitation is similar to that observed in the left atrium with chronic mitral regurgitation. Direct measurement of right atrial pressure demonstrates a marked increase in pressure with the very onset of systole, thereby producing a tall "v" wave (figure 8 and waveform 7). Since the "c" wave may not be apparent, this has also been termed a "c-v" or an S wave; it is proportional to the severity of regurgitation in most patients. As with left atrial or pulmonary wedge pressures, "v" waves on the right side of the heart are determined by the pressure-volume compliance characteristics of the chamber. As a result, severe angiographic regurgitation may be present with minimal "v" waves.

During systole in tricuspid regurgitation, the right ventricle and right atrium are in direct communication. However, despite the large volume of blood in the right atrium, the mean right atrial pressure may be normal or only slightly increased; this is largely a result of a very complaint right atrium. The amplitude of the tall "v" wave is therefore less than the amplitude of that observed in right ventricular systole. In addition, the amplitude of the "a" wave is frequently reduced because of right atrial distension and reduced contractility. The right atrial diastolic pressure is normal and is similar to the left ventricular diastolic pressure.

The effects of tricuspid regurgitation on the right atrium and inferior vena cava can be assessed by measuring two pressures simultaneously, one from each of the two lumens of a balloon-tipped pulmonary artery catheter. The waveform of the inferior vena cava is slower in upstroke and in downstroke and is associated with reduced velocity. The blunted waveform is due, in part, to the considerably higher capacity and compliance of the vena cava compared with that of the right atrium. In addition, the mean right atrial pressure is lower than that in the vena cava, with a 2 to 4 mmHg pressure gradient required for maintenance of normal blood flow. The pressure gradient between the inferior vena cava and right atrium occurs predominantly during the end of atrial diastole (figure 8). In most cases, superior vena cava flow has a time course similar to inferior vena cava flow.

Jugular venous pulsation — The jugular venous pulsation closely reflects events in the right atrium and the venae cavae [17,18]. However, the change in pressure within the right atrium is reflected principally by a change in volume for the venous system. Tricuspid insufficiency often produces a prominent "v" wave that begins early, tending to obliterate the "x" descent. In severe tricuspid regurgitation, the "v" wave begins with the "c" wave and shows a broad plateau, terminating in a steep "y" descent. This wave has been termed the regurgitant or "s" wave. However, neither prominent "v" waves (>15 mmHg) or an elevated mean right atrial pressure (>12 mmHg) can reliably predict the presence of moderate or severe tricuspid regurgitation although their absence is predictive of its absence [19].

In the setting of atrial fibrillation, nearly complete obliteration of the "x" descent is required before the diagnosis of tricuspid insufficiency may be made from a venous pulse wave. With normal sinus rhythm, changes in the venous pulse may be only a slight decrease in the "x" descent equal or above the level of the "y" trough. In some patients, a separate systolic wave may appear on the "v" wave ascent and be a clue (albeit obscure) to the presence of tricuspid regurgitation [15].

A normal jugular venous pulse cannot be used to exclude tricuspid disease, since regurgitation may infrequently be associated with a relative normal venous pulse wave. In this setting, although the characteristic pulse waves may be absent at rest, they may be elicited by inspiratory maneuvers or an increasing heart rate [15]. The 2020 American College of Cardiology/American Heart Association guidelines for valvular heart disease note that in patients with tricuspid regurgitation, invasive measurement of the cardiac index, right-sided diastolic pressures, pulmonary artery pressures, and pulmonary vascular resistance, as well as right ventriculography, can be useful when clinical and noninvasive data are discordant or inadequate [2].

TRICUSPID STENOSIS — As with the hemodynamic abnormalities observed in mitral stenosis, tricuspid stenosis produces an obstruction of blood flow from the right atrium to the right ventricle, resulting in a diastolic gradient between these two chambers.

Right atrial pressure — Because of the impairment to blood flow during diastole, the volume of blood in the right atrium and the mean right atrial pressure is increased. After tricuspid valve opening, the pressure slowly decreases and the "y" descent is gradual. The "a" wave is markedly increased because of the stenosis.

Right ventricular pressure — Since the valve abnormality is proximal to the right ventricle, the pressure waveforms are normal except for a reduced amplitude of the "a" wave. The right ventricular end-diastolic pressure may be lower than normal because of the impaired filling of the right ventricle from the right atrium.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)

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SUMMARY AND RECOMMENDATIONS

●Echocardiography is the primary modality for diagnosis and evaluation of valvular disease. In a small minority of patients, further evaluation with invasive intracardiac pressure measurements and/or angiography is needed because the echocardiographic data are nondiagnostic or discrepant with clinical findings. (See 'Introduction' above.)

●Aortic valve disease

•Cardiac catheterization is recommended for hemodynamic assessment of aortic stenosis in older adults only in symptomatic patients in whom noninvasive tests are inconclusive or provide discrepant results. There is some risk of cerebral embolization associated with crossing a calcific stenotic aortic valve. (See 'Aortic stenosis' above.)

•A precise assessment of the aortic valve gradient can be obtained by the simultaneous measurement of the aortic pressure (as assessed with a pigtail catheter above the aortic valve), and the left ventricular (LV) pressure (measured using the transseptal technique or using dual lumen fluid filled catheter or for research dual high fidelity transducer catheter) (figure 1). (See 'Aortic valve gradient' above.)

•The aortic pressure tracing in aortic regurgitation reveals a rapid upstroke (due to augmented LV contractility) and an increased systolic pressure (due to increased stroke volume) and a rapid fall to a low diastolic pressure (yielding a widened pulse pressure). (See 'Chronic aortic regurgitation' above.)

•With acute aortic regurgitation, there is a steep rise in LV diastolic pressure and a markedly elevated LV end-diastolic pressure (which is equivalent to the aortic end-diastolic pressure). Since forward stroke volume declines, aortic systolic pressure is reduced and the pulse pressure is therefore smaller. (See 'Acute aortic regurgitation' above.)

●Mitral valve disease

•With chronic mitral regurgitation, the regurgitant flow produces a large left atrial pressure wave immediately with the onset of ventricular systole (waveform 4). During the initial part of diastole, the left atrium rapidly decompresses with a large antegrade flow to the LV. (See 'Chronic mitral regurgitation' above.)

•With acute mitral regurgitation, the left atrial pressure rises abruptly with the onset of systole, causing a very tall "v" wave. Because of this "v" wave, the pressure gradient between the left atrium and LV declines by the end of systole; the amplitude of the "v" wave and that of LV systole are nearly equivalent. (See 'Acute mitral regurgitation' above.)

•The severity of mitral stenosis as reflected by the mean mitral valve gradient (MVG) is measured during diastole by the simultaneous comparison of the LV pressure (obtained with an LV catheter positioned retrogradely from the aorta), and the left atrial pressure (measured directly using a transseptal catheter or indirectly with a pulmonary artery catheter in the wedged position [PCWP]) (waveform 6). (See 'Mitral valve gradient' above.)

●Tricuspid valve disease

•Tricuspid regurgitant flow produces a distinct right atrial pressure waveform with the transmission of the regurgitant wave into the right atrium, the vena cava, and ultimately the jugular veins (waveform 7). (See 'Tricuspid regurgitation' above.)

•Tricuspid stenosis produces an obstruction of blood flow from the right atrium to the right ventricle, resulting in a diastolic gradient between these two chambers. (See 'Tricuspid stenosis' above.)