A multi-panel scientific visualization showing subtomogram averages and molecular docking models of the cardiac muscle sarcomere's C-zone, specifically focusing on the interactions between myosin thick filaments and actin thin filaments. Panel (a) provides a cross-sectional view of a central myosin filament (M) surrounded by six actin filaments (A1, A2), illustrating the threefold symmetry of the thick filament backbone. Panels (b-g) integrate structural models to characterize MyBP-C (myosin-binding protein C) and myosin head arrangements. Longitudinal stereo views (c-e) demonstrate the axial distribution of myosin crossbridge 'crowns' (Crowns 1, 2, and 3) along the 430 Å repeat, with Crown 1 coinciding with the MyBP-C stripe. The models incorporate Ig-domain spheres (red) to trace the path of MyBP-C from the myosin backbone to actin, alongside docked crystal structures of cardiac thick filaments (yellow) and myosin motor domains (pink/cyan). This diagram serves as a high-resolution anatomical and physiological illustration for understanding cardiac muscle contraction at the molecular level, highlighting the spatial relationship between titin, MyBP-C, and the actomyosin complex.

This physiological diagram illustrates simulated calcium dynamics in rat ventricular myocytes, focusing on the mechanisms of excitation-contraction coupling. The image is divided into five panels (A-E) tracking parameters over a 1.0-second timeline. Panel A (Ca2+ sparks) shows high-amplitude calcium spikes in the dyadic subspace ([Ca2+]ds) reaching ~100 µM. Panel B (Ca2+ quarks) displays lower-amplitude, high-frequency [Ca2+]ds fluctuations below 10 µM, representing 'invisible' leak events. Panel C tracks the dynamics of junctional sarcoplasmic reticulum (jSR) calcium release ([Ca2+]jsr), demonstrating local depletion following release events. Panel D quantifies the number of Ryanodine Receptor (RyR) openings, ranging from 0 to 50. Panel E illustrates the concentration of calcium-bound calmodulin complex ([CaCm2+]ds). These charts demonstrate the stochastic nature of calcium release units (CRUs) and the correlation between RyR channel opening and subspace calcium elevation. The data is relevant to cardiac electrophysiology, specifically the study of cardiac alternans and intracellular calcium signaling in cardiomyocytes.

A two-panel (A and B) pathophysiology diagram illustrating motor neuron signaling, excitation-contraction coupling (ECC), and (neuro)endocrine skeletal muscle responses. Panel A depicts the neuromuscular junction where an action potential triggers ECC and the release of intramyocellular calcium (Ca2+), leading to myofiber contraction. It also shows Ca2+ activating signaling pathways (CaMK, CnA) that modulate transcriptional factors (CREB, ATF2) and the coactivator PGC-1̑ in the nucleus, alongside retrograde feedback to the motor neuron via neurotrophic factors (NTs). Adrenergic signaling through ̒2-adrenoreceptors (̒2 AR) from the sympathetic nervous system is also represented. Panel B focuses on 'exerkines,' showing the secretion of myokines and myobolites from the muscle cell. It classifies signaling effects as autocrine, paracrine (e.g., GDF3, IL-13, Lactate), and endocrine. Endocrine factors listed include adipokines, hepatokines, osteokines, corticosteroids, testosterone, and growth hormone-regulated IGF-1, highlighting the systemic coordination between muscle, liver, adipose, and bone tissues during contractile activity.

This composite educational graphic illustrates multiparametric optical mapping of cardiac excitation-contraction coupling in an isolated heart model. Panels A and B present isochronal activation maps for transmembrane voltage (Vm) and intracellular calcium (Ca), respectively, showing impulse propagation from the apex (blue) to the base (red) over a 45 ms scale. Panel C displays representative signal upstroke traces, highlighting the physiological lag between electrical depolarization (Vm) and calcium release (Ca) at both the apex and base. Panel D provides a bar chart comparing transverse (T) and longitudinal (L) conduction velocities for Vm and Ca, indicating significantly faster longitudinal Vm propagation compared to Ca. Panels E and F show sequential time-lapse frames (t=0 to 40 ms) of wavefront propagation following electrical pacing at the apex (indicated by arrows). These frames demonstrate the development of spatial heterogeneity and wavebreak in the calcium channel at t=40 ms, serving as a model for studying electrophysiological discontinuities and potential arrhythmogenic precursors.

This medical graphic presents a multi-subject comparative study (8 subjects) of cardiovascular mechanics, combining biventricular displacement maps and pressure-volume (PV) loops. The top portion of each subject panel shows 3D color-coded ventricular models during end-systole and end-diastole. Displacement is mapped on a scale from 0 cm (blue) to approximately 1.2–1.6 cm (red), illustrating wall motion across the cardiac cycle. Below each set of models, PV loops represent ventricular hemodynamics. These loops compare left ventricle (LV, green) and right ventricle (RV, purple) data. Solid lines represent computational simulations, while dotted lines represent clinical measurements. The data demonstrates the relationship between pressure (mmHg) and volume (mL), facilitating an assessment of contractility, ejection fraction, and stroke work. The variety in loop morphology and displacement patterns across the subjects highlights patient-specific pathological states, likely in the context of Pulmonary Arterial Hypertension (PAH), where RV remodeling and displacement abnormalities are clinically significant.

Summary : This figure shows a pressure–volume loop for the left ventricle, illustrating how ventricular volume and pressure change during the cardiac cycle, with key phases and valve events annotated. The isovolumetric relaxation and contraction periods are highlighted, and systolic/diastolic blood pressures are marked. pressure–volume loop diagram: # Title & Axes : • No explicit title on the figure, but the legend describes it as a "Pressure–volume loop demonstrating changes in ventricular volume during filling and ejection with corresponding changes in intracavity pressure." • X-axis: "Left ventricular volume (mL)" with tick marks at 0, 20, 40, 60, 80, 100, 120, 140, 160. • Y-axis: "Left ventricular pressure (mmHg)" with tick marks at 0, 20, 40, 60, 80, 100, 120, 140. • Additional axis labels: "Left ventricular end-diastolic pressure" (blue, left), "End-diastolic volume" (blue, bottom right), "Stroke volume" (black, bottom center). # Phases & Events : • Isovolumetric relaxation: vertical line at low volume, pressure drops, labeled. • Diastolic filling: horizontal line at low pressure, volume increases, labeled. • Isovolumetric contraction: vertical line at high volume, pressure rises, labeled. • Ventricular ejection: curved line, volume decreases as pressure peaks and falls, labeled. • Valve events: – Mitral valve opens (bottom left corner, low pressure/volume). – Mitral valve closes (bottom right corner, high volume/low pressure). – Aortic valve opens (top right corner, high volume/high pressure). – Aortic valve closes (top left corner, low volume/high pressure). # Blood Pressure Markers : • Systolic BP: horizontal dashed blue line at ~120 mmHg. • Diastolic BP: horizontal dashed blue line at ~80 mmHg. # Design Encodings : • Black solid lines for the loop. • Blue dashed lines for blood pressure markers. • Blue text for end-diastolic volume/pressure. • Labeled arrows for direction of phases and valve events. # Analysis : • The loop traces the cardiac cycle, starting at low pressure/volume (end-systolic), filling during diastole, rising sharply during isovolumetric contraction, ejecting blood during ventricular ejection, and dropping pressure during isovolumetric relaxation. • Systolic and diastolic blood pressures are marked, showing the pressure range during ejection. • The width of the loop (horizontal distance) represents stroke volume. • The figure clearly distinguishes the four main phases and the timing of valve openings/closings, providing a comprehensive view of ventricular mechanics during a heartbeat.

Educational composite figure demonstrating multimodal assessment of left ventricular (LV) function and volume. Panel A shows a Pressure-Volume (PV) loop graph plotting LV pressure (mmHg) against LV volume (mL), characteristic of cardiac cycle analysis. Panel B displays Cardiac Magnetic Resonance Imaging (CMRI) in a 2x4 grid comparing end-diastolic and end-systolic phases across four planes: short-axis apex, papillary muscle level, basal level, and long-axis view. These views highlight ventricular wall thickening and chamber reduction during systole. Panel C illustrates Three-Dimensional Echocardiography (3DE) including apical 4-chamber, apical 2-chamber, and short-axis views alongside a computed 3D reconstruction of the LV volume. The contrast between end-diastolic and end-systolic frames in both CMRI and 3DE allows for the calculation of stroke volume and ejection fraction. The figure serves as a comparative reference for diagnostic imaging modalities used in cardiology to quantify cardiac remodeling and performance after myocardial injury.

This physiological waveform graph displays cardiac simulator signals at a heart rate of 80 bpm, illustrating hemodynamic relationships across the cardiac cycle over a 5-second interval. The upper panel tracks Pressure (mmHg), comparing Left Ventricular Pressure (LVP) and Aortic Pressure (AoP). The LVP waveform shows cyclical rises to approximately 150 mmHg during systole, falling near 0 mmHg in diastole. The AoP oscillates between roughly 105 and 130 mmHg, with distinct high-frequency spikes (dicrotic notches/oscillations) occurring at the moment of mechanical aortic valve closure. The lower panel displays Aortic Root Flow (AoF) in L/min, showing pulsatile flow synchronized with pressure changes. Flow peaks at approximately 20 L/min during the rapid ejection phase and exhibits a brief negative deflection (backflow) to roughly -8 L/min, indicating closure of the aortic valve. These waveforms serve as a diagnostic algorithm illustration for understanding the relationship between chamber pressure, arterial pressure, and forward stroke volume in cardiovascular physiology.

Summary : This figure compares cardiac function under two conditions using two types of plots: (A) the Frank-Starling relationship between stroke volume and left ventricular filling, and (B) pressure-volume loops with end-systolic elastance (Ees) lines. line and schematic plot: # Panel A: Frank-Starling Curve : • Y-axis: Stroke Volume (no units shown). • X-axis: LVEDP or LVEDV (Left Ventricular End-Diastolic Pressure or Volume; no units shown). • Two curves are shown: – Curve 1: Higher, solid line, labeled "1". – Curve 2: Lower, dashed line, labeled "2". • Each curve has a point marked (solid dot) on it. # Panel B: Pressure-Volume Loop and End-Systolic Elastance : • Y-axis: Pressure (no units shown). • X-axis: Volume (no units shown). • Two pressure-volume loops: – Loop 1: Solid line, larger, leftward, labeled "1". – Loop 2: Dashed line, smaller, rightward, labeled "2". • Two Ees (end-systolic elastance) lines: – Ees 1: Steeper, solid line, labeled "1". – Ees 2: Less steep, dashed line, labeled "2". # Design Encodings : • Solid lines for condition 1, dashed lines for condition 2. • Dots mark specific points on the curves in panel A. • Pressure-volume loops are outlined, with loop 2 shown as a dashed outline. # Analysis : • Panel A shows that condition 1 (solid line) has a higher stroke volume for any given LVEDP/LVEDV compared to condition 2 (dashed line), indicating better cardiac function. • Panel B shows that condition 1 has a larger, leftward pressure-volume loop and a steeper Ees line, indicating greater contractility. Condition 2 has a smaller, rightward loop and a less steep Ees line, indicating reduced contractility. • The figure visually contrasts normal/enhanced versus impaired cardiac function using both stroke volume response and pressure-volume relationships.

This clinical photograph shows a close-up, lateral view of the right side of an elderly patient's neck, focusing on the lower cervical region. A white arrow points to a distinct, localized swelling located along the anterior border of the right sternocleidomastoid muscle. Visible distension and prominence of the right external jugular vein are observed, suggesting impaired venous return or increased central venous pressure. The overlying skin exhibits age-related changes, including fine wrinkling and solar lentigines. Clinically, these findings represent external manifestations of venous congestion, which may be secondary to superior vena cava syndrome or right atrial compression, leading to internal jugular vein thrombosis. This image serves as an educational example of physical signs associated with thoracic or abdominal masses impacting cardiac inflow.

**Imaging Modality:** Cardiac Magnetic Resonance Imaging (MRI), axial steady-state free precession (SSFP) sequence. **Anatomical Region and Landmarks:** Mediastinum and thoracic cavity showing the heart and great vessels in a patient with tricuspid atresia and prior atriopulmonary Fontan palliation. **Observed Pathology:** Severe, aneurysmal dilatation of the right atrium (measuring approximately 7 x 7.5 cm). The massive enlargement of the right atrium causes significant mass effect and posterior displacement of adjacent structures. **Characteristic Visual Features:** - **Atrial Morphometry:** Markedly enlarged, globular right atrium dominant within the thoracic cross-section. - **Vascular Impingement:** The dilated right atrium exerts direct extrinsic compression on the pulmonary venous return pathways. - **Ventricular Morphology:** Single functional ventricle consistent with the surgical history of tricuspid atresia. - **Signal Characteristics:** Blood pool demonstrates typical hyperintense signal on SSFP, highlighting the disproportionate size of the atrial chamber relative to the ventricular mass and the restricted space for pulmonary veins. **Diagnostic Context:** This appearance is characteristic of late complications following an atriopulmonary Fontan connection, where chronic pressure and volume overload lead to progressive giant atrial enlargement and secondary obstructive effects on systemic or pulmonary venous return.