Physiological insights of recent clinical diagnostic and therapeutic technologies for cardiovascular diseases

Abstract

Diagnostic and therapeutic methods for cardiovascular diseases continue to be developed in the 21st century. Clinicians should consider the physiological characteristics of the cardiovascular system to ensure successful diagnosis and treatment. In this review, we focus on the roles of cardiovascular physiology in recent diagnostic and therapeutic technologies for cardiovascular diseases. In the first section, we discuss how to evaluate and utilize left ventricular arterial coupling in the clinical settings. In the second section, we review unique characteristics of pulmonary circulation in the diagnosis and treatment of pulmonary hypertension. In the third section, we discuss physiological and anatomical factors associated with graft patency after coronary artery bypass grafting. In the last section, we discuss the usefulness of mechanical ventricular unloading after acute myocardial infarction. Clinical development of diagnostic methods and therapies for cardiovascular diseases should be based on physiological insights of the cardiovascular system.

Keywords: Cardiovascular physiology; Coronary artery bypass grafting; Left ventricular arterial coupling; Left ventricular assist device; Pulmonary circulation.

Fig. 1

Ventricular pressure–volume relationship. ESPVR end-systolic pressure–volume relationship, Pes end-systolic arterial pressure, Ves end-systolic left ventricular volume, Ved end-diastolic left ventricular volume, V ₀ the volume-axis intercept of ESPVR, Ees end-systolic left ventricular elastance, Ea effective arterial elastance, SV stroke volume

Fig. 2

Schematic representation of a framework of single-beat end-systolic left ventricular elastance (Ees) estimation by approximating the time-varying elastance curve as two linear functions. a Time-varying elastance curve (solid line) and two linear approximations (dashed line). b Estimated end-systolic pressure–volume loop (solid line). LV left ventricle, Ead elastance at the end of isovolumic contraction phase, Eed end-diastolic elastance, PEP pre-ejection period, ET ejection time, θiso and θej angles of approximated lines of isovolumic contraction phase and ejection phase, respectively, Pmax peak isovolumic pressure, Pad pressure at the end of isovolumic contraction phase, Ped end-diastolic pressure

Fig. 3

Upper panels, scatter plot (a) and Bland–Altman plot (b) to analyze the correlation between ventricular arterial coupling (Ees/Ea) obtained by the original method using end-systolic arterial pressure (Pes), expressed as Ees/Ea, and Ees/Ea approximated using mean arterial pressure (Pm), expressed as (Ees/Ea)′. Lower panels, scatter plot (c) and Bland–Altman plot (d) to analyze the correlation between ventricular arterial coupling (Ees/Ea) obtained using end-systolic arterial pressure (Pes), expressed as Ees/Ea, and the adjusted values of (Ees/Ea)′ [approximated using mean arterial pressure (Pm)] expressed as adj(Ees/Ea)′

Fig. 4

Age distribution of ventricular arterial coupling (Ees/Ea) in males (open circles) and females (closed circles). The overall mean value and standard deviation (SD) is 1.2 ± 0.6

Fig. 5

Computation of pulmonary input impedance. a, b Pressure and flow waveforms, respectively, recorded simultaneously. c Characteristic impedance (Zc) obtained from the instantaneous pulmonary pressure–flow plot (time domain manner) [13]. d, e Modulus and phase angle of the pulmonary input impedance computed from decomposed Fourier transform of pressure and flow, respectively

Fig. 6

The pressure–flow relationship of the pulmonary artery. In normal subjects, increase in trans-pulmonary pressure (PAP-PAOP) is suppressed in the high flow range. The angles of θ1 and θ2 indicate pulmonary artery resistance (PVR) at cardiac output of 2 and 10 l/min, respectively. PVR varies with change in cardiac output even in the same subject [33]. In patients with pulmonary hypertension (PH), this regression curve becomes steeper, reflecting impaired pulmonary vascular autoregulation against increased flow. PAP mean pulmonary artery pressure, PAOP pulmonary artery occlusion pressure

Fig. 7

Computation of end-systolic elastance (Ees) of the right ventricle. a Peak isovolumic pressure (Pmax) from a given single contraction of the right ventricle is estimated from the extrapolated sine curve (dashed line) using the isovolumic pressure (shadowed periods) [42, 43]. b Ees is estimated by combining the Pmax, the right ventricular end-systolic pressure (Pes) and stroke volume (SV) [43]. The estimated pressure–volume loop of the right ventricle is drawn with a dashed line. Ea effective arterial elastance, HMP hydromotive pressure, ICT isovolumic contraction time, IRT isovolumic relaxation time

Fig. 8

Schematic representation of wall shear stress. Wall shear stress (τ _w) is calculated as shear stress at y = 0. μ dynamic viscosity, u(y) flow velocity along the boundary, y the distance from the boundary

Fig. 9

Schematic representation of two percutaneous LVADs. Impella^® (a) pulls blood from the left ventricle into the ascending aorta. TandemHeart™ (b) pumps blood from the left atrium into one or both femoral arteries

Fig. 10

a Pressure–volume area (PVA) indicated by the gray area is the sum of external work (EW) and potential energy (PE). PVA couples with myocardial oxygen consumption. b Theoretical analysis of the impact of left ventricular assist device (LVAD) on the pressure–volume (PV) loops. The loop in solid line represents the baseline PV loop. In partial LVAD support, LVAD decreases left ventricular end-diastolic volume and increases mean arterial pressure, which in turn increases end-systolic volume (loop in dashed line). On the other hand, total LVAD support markedly lowers left ventricular pressure to below the arterial pressure, yielding an extremely small PVA (loop in bold line). EDPVR end-diastolic pressure volume relation, ESPVR end-systolic pressure volume relation, V0 the volume-axis intercept of ESPVR, Vu the volume-axis intercept of EDPVR