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Inflammation affecting tissue of the heart. The term is broad: specifying endocardium, myocardium or pericardium identifies anatomically different processes that can have different consequences.

C. E. Nerantzis is an author of anatomical research on coronary arteries and their distribution in the human heart. The 1996 primary paper Functional dominance of the right coronary artery: incidence in the human heart by C. E. Nerantzis and others lists the author with the Pathology Department, University of Athens. Its byline establishes the initials used here; it does not by itself establish a fuller personal name.^[ref]

Nerantzis and colleagues studied 200 human hearts after injection of radiopaque material, combining direct observation with X-ray analysis. They classified 178 as right dominant because the right coronary artery gave rise to the posterior interventricular artery. Within those 178, they distinguished 19 specimens with both a large posterior branch and a large continuation beyond the crux. The mapped right coronary artery in this subgroup supplied the right ventricle and nearly half the left ventricle.^[ref]

The nested counts show why a classification and a detailed territory map are different observations: $178/200=89\%$ of this collection met the usual right-dominance criterion, but the described extended subgroup was $19/178\approx 10.7\%$ of those right-dominant hearts. These sample fractions do not automatically estimate every population. The work illustrates how coronary dominance summarizes a branch origin while leaving additional variation in arterial extent.

Radiopaque filling makes the vessel paths visible; it does not directly measure living blood flow under exercise or after an obstruction. The anatomical observation motivates questions about which myocardium a proximal lesion could affect, while physiological flow and clinical outcome require additional evidence.

A chemical synapse transmits a signal by releasing neurotransmitter from a presynaptic neuron to act on postsynaptic receptors across a synaptic cleft. The two cell membranes remain separate. A typical fast transmission sequence is:

See Chemical Synapses and 3.1 Synapses. The fast pathway uses synaptic vesicles prepared near release sites; it does not require a distant synaptic vesicle to travel across the terminal after every action potential. See Basic Neurochemistry: calcium entry and vesicles at release sites. Some chemical synapses release neurotransmitter in response to graded presynaptic membrane potential changes rather than action potentials.

Neurotransmitter clearance limits how long released neurotransmitter remains available. Depending on the neurotransmitter and location, diffusion away, uptake through membrane transport proteins into the sending or neighboring biological cells, and breakdown by enzymes contribute. Receptor binding and unbinding also affect response duration. Recovering synaptic vesicle membrane is a separate recycling task; uptake of released neurotransmitter is not the return of an intact synaptic vesicle. See General Principles of Cell Communication.

This electrical-to-chemical-to-electrical sequence offers several places to adjust a signal: synaptic release probability, receptor availability and neurotransmitter clearance can change its strength or duration. It helps explain why synaptic plasticity can modify communication between neurons, and why an arriving action potential need not cause a postsynaptic action potential.

Otto Loewi's 1936 Nobel lecture describes his 1921 experiment: fluid from a frog heart whose nerves had been stimulated produced the corresponding response when transferred to another heart. The transferable substance established chemical mediation in that preparation. This was evidence for released chemical signaling, not yet an identification of synaptic vesicle fusion and not a claim that every synapse is chemical. See Loewi, The Chemical Transmission of Nerve Action, Nobel lecture, 12 December 1936.

Coauthor of research identifying ISL1-positive cardiac progenitors. The study connected a molecularly defined cell population with proliferation before differentiation and contribution to the developing heart.^[ref]

Christopher M. Kramer is a cardiologist whose research uses cardiovascular magnetic resonance imaging to assess the heart. His University of Virginia profile identifies cardiovascular imaging as an area of expertise.^[ref] He is the first author of the 2020 primary protocol document specifying standardized cardiovascular magnetic resonance imaging acquisitions.^[ref]

One concrete contribution of such a protocol is to make image geometry reproducible. Its left-ventricular procedure links the cardiac apex, mitral valve center, cardiac long axis views and a cardiac short-axis stack.^[ref] The geometry determines which anatomy is acquired before an analyst draws a cavity boundary.

An original example explains the measurement consequence. A volume reconstructed as $V\simeq {\sum }_i{A}_i\Delta z_i$ depends on both the cavity areas and the represented slice thicknesses. If ten slices each have area 8 cm${}^2$ and represented thickness 0.8 cm, the estimate is 64 mL. Omitting one such slice loses 6.4 mL even if every retained boundary is traced perfectly. Standardized coverage and phase selection therefore address errors that cannot be removed merely by improving image segmentation on the available slices.

The documented protocol work connects acquisition choices to interpretable measurements of chamber structure and function. It provides technical procedures and reference geometry; the arithmetic example here illustrates their purpose rather than reporting a result from that document.

The circulatory system transports blood through the heart and vessels, connecting exchange surfaces with tissues. In humans, pulmonary and systemic pathways operate in series. Pressure gradients drive flow, while the distribution of resistance helps determine how total output is divided among organs.

The circumflex artery is a major branch of the left coronary artery that follows the coronary sulcus around the left side of the heart. It gives branches including a left marginal branch.^[ref] It is distinct from the left anterior descending artery, the other typical major left-coronary branch.

Its route can also be relevant to posterior supply. When the posterior descending artery originates through the circumflex system, that connection contributes to a left-dominant coronary dominance pattern. A posterior branch name therefore does not uniquely identify a right-coronary origin.

The network distinction helps interpret where a finding lies. A segment before the left-coronary bifurcation is upstream of both major branches. A segment within the circumflex route is downstream of that split. These are different anatomical positions even though both may be described broadly as left-coronary findings.

An original two-outlet model assigns left-coronary flow $Q_L=Q_A+Q_C$, where $Q_A$ is anterior-branch flow and $Q_C$ circumflex flow. Knowing $Q_L=180\mathrm{mL}\mathrm{mi}{\mathrm{n}}^{-1}$ does not determine $Q_C$: pairs $(Q_A,Q_C)=(110,70)$ and $(90,90)$ produce the same total. An additional branch-sensitive observation is required.

Actual arterial mapping can be examined by selective contrast imaging. The primary Judkins method used selective catheterization with serial and cine recording.^[ref] Such observation identifies a route and its geometry; interpreting coronary blood flow or oxygen supply also requires the relevant physiological measurements.

Continuous-wave Doppler echocardiography measures the Doppler frequency distribution of continuously transmitted and received ultrasound through the heart. It can record high flow velocities without the pulse-repetition-frequency aliasing limit of pulsed-wave Doppler echocardiography, but it does not select one depth along the beam. Signals from different contributing locations can overlap.^[ref]

For an aligned flow at speed $v$, the leading Doppler ultrasound relation isWith stipulated transmitted frequency $f_0=2\mathrm{MHz}$, sound speed $c=1540m/s$ and $v=4m/s$, the shift is approximately $10.4\mathrm{kHz}$. A pulsed measurement with pulse repetition frequency $4\mathrm{kHz}$ would have a Doppler Nyquist frequency of only $2\mathrm{kHz}$. Continuous-wave acquisition avoids that particular pulse-rate restriction. Its receiving electronics and digital sampling still have finite bandwidth; continuous transmission does not imply unlimited measurable frequency.

The price is Doppler range ambiguity. If a beam intersects two moving regions, a peak in the spectrum does not by itself label which depth produced it. The anatomical image, direction, timing and waveform context supply additional evidence. The outer spectral envelope describes the fastest detected motion along the beam, rather than a direct spatial average over one known vessel opening.^[ref]

This matters when estimating stroke volume. Multiplying a continuous-wave peak-velocity integral by an arbitrarily selected area can combine measurements from different sites or different parts of a velocity distribution. Flow-profile mismatch in Doppler stroke-volume estimation explains the separate requirement that the chosen velocity represent the area used in the volume calculation.

A coronary artery is an artery supplying the heart's own tissues, especially the myocardium. The main left coronary artery and right coronary artery arise from the proximal aorta near the aortic valve. Their branches supply the working cardiac muscle rather than merely conveying blood through the heart's chambers.^[ref]

This arrangement separates two circulations that can otherwise be confused. Blood inside a cardiac chamber is being pumped onward; coronary blood flow brings oxygen and other materials to the living wall doing the pumping. An open chamber and a patent large coronary artery therefore answer different anatomical questions. Distribution through smaller vessels and exchange with tissue also matter.

An original conservation calculation illustrates the supply problem. If coronary volume flow is $Q$ and arterial oxygen content is $C_a$, then coronary oxygen delivery isWith chosen values $Q=250\mathrm{mL}\mathrm{mi}{\mathrm{n}}^{-1}$ and $C_a=0.20\mathrm{mL}{\mathrm{O}}_2\mathrm{m}{\mathrm{L}}^{-1}$, delivery is $50\mathrm{mL}{\mathrm{O}}_2\mathrm{mi}{\mathrm{n}}^{-1}$. If a representative venous oxygen content is $C_v=0.08\mathrm{mL}{\mathrm{O}}_2\mathrm{m}{\mathrm{L}}^{-1}$, a steady-state inflow–outflow balance givesHere $E$ is the coronary oxygen extraction fraction. The example assumes matched inflow and outflow from the same represented tissue, with negligible oxygen accumulation; these are illustrative values, not clinical reference limits. Delivery and extraction distinguish a flow measurement from the tissue's oxygen use.

Vascular stenosis can change the supply route, while the observed consequence depends on more than one geometric percentage. Coronary angioplasty targets a narrowed arterial segment. The historical primary study measured both stenosis and the pressure difference across the affected region, making anatomy and a physiological observation available together.^[ref] Neither observation by itself supplies all the information in the oxygen balance above.

Disease of the arteries supplying the heart muscle, commonly involving atherosclerotic narrowing. Limitation of blood supply can produce ischaemia, while the presence of a lesion and its immediate functional effect are separate questions.

The coronary circulation supplies and drains the heart's own tissue. Coronary arteries branch from the aorta to supply the myocardium; cardiac veins return blood toward the right atrium.^[ref] Blood moving through a ventricular cavity is not the same flow as blood perfusing the surrounding muscle.

Much coronary venous return passes through the coronary sinus, while anterior cardiac veins provide a direct route to the right atrium.^[ref] Consequently a coronary-sinus sample represents its drainage territory rather than automatically every part of the heart. Anatomical pathways must match the region whose blood flow and oxygen uptake are being estimated.

An original tissue-balance example uses regional flow $Q=80\mathrm{mL}\mathrm{mi}{\mathrm{n}}^{-1}$, arterial oxygen content $C_a=0.20\mathrm{mL}{\mathrm{O}}_2\mathrm{m}{\mathrm{L}}^{-1}$ and matching venous oxygen content $C_v=0.08$ in the same units. Then regional coronary oxygen uptake isThe arterial delivery rate is $Q{C}_a=16$ in those units. Delivery and uptake differ because oxygen remains in the returning blood. The values are stipulated, not normal-reference limits.

A primary 2007 experiment measured coronary volumetric flow using continuous saline thermodilution, an infusion catheter and a pressure/temperature guidewire, with comparisons in dogs and patients.^[ref] This provides a concrete way to investigate the flow term; it does not by itself measure the oxygen-content difference.

The arterial map also varies among hearts. A radiopaque-injection study classified 178 of 200 examined hearts as right dominant by the origin of the posterior interventricular artery.^[ref] Dominance names an anatomical branching criterion, not a claim that one artery supplies the entire heart.

Disorder of the small vessels supplying the heart muscle. Impaired regulation of local flow can cause ischemia even when the major coronary arteries lack a large obstructing lesion.^[ref]

The coronary sinus is a major venous collecting channel of the heart that opens into the right atrium. It receives blood from cardiac veins, including the great cardiac vein, middle cardiac vein and small cardiac vein.^[ref] It belongs to the venous return pathway, distinct from the coronary arteries supplying the myocardium.

The collecting-channel arrangement explains its use in a regional balance. Incoming flows combine before the sample or outflow observation is taken. In a steady model with negligible local storage,If represented inflows are $90$ and $30\mathrm{mL}\mathrm{mi}{\mathrm{n}}^{-1}$, the sinus outflow is $120\mathrm{mL}\mathrm{mi}{\mathrm{n}}^{-1}$. This is a chosen continuity example, not a normal flow value.

A measurement at the coronary sinus does not automatically represent every myocardial route. If another modeled pathway returns $10\mathrm{mL}\mathrm{mi}{\mathrm{n}}^{-1}$ directly to a chamber, the total venous return from the represented heart is $130$, while the sinus observation remains $120$. Treating the latter as the whole total would miss about $7.7\%$ in this example.

Likewise, venous oxygen content sampled from a collecting channel is a mixture weighted by its contributing flows. It should be paired with flow and arterial measurements representing compatible tissue when calculating coronary oxygen uptake. Knowing the sampling site is part of defining the biological quantity, not simply a label attached after measurement.

The coronary sulcus is the external groove around the heart at the boundary between its atria and ventricles. It provides a route for parts of the right coronary artery, circumflex artery, great cardiac vein and coronary sinus.^[ref]

An anatomical route can be reconstructed from connected landmarks: the great cardiac vein runs from the anterior interventricular sulcus into the coronary sulcus and toward the coronary sinus. The turn distinguishes a vessel following the atrial–ventricular boundary from one continuing toward the cardiac apex. This is useful when relating an anterior view to a posterior view of the same specimen.

The groove should not be treated as a rigid pipe carrying all of these vessels in one fixed order. In a primary dissection series, the great cardiac vein's relationship to the neighboring arteries differed among specimens.^[ref] A diagram can therefore correctly show the main route while suppressing variation in crossings and spacing. The coronary sulcus describes surface geography; identifying a particular artery or vein still requires tracing its connections.

Dilated cardiomyopathy is a form of cardiomyopathy involving enlargement of a ventricular chamber together with impaired pumping by the heart muscle. The left ventricle is a central site of the disorder, and other chambers can also be affected. Enlargement and pumping function are related but distinct observations; chamber size alone does not determine how much blood is expelled.^[ref]

A simple volume example makes that distinction quantitative. Let end-diastolic volume be $V_{\mathrm{ED}}$ and end-systolic volume be $V_{\mathrm{ES}}$. ThenHere SV is stroke volume and EF is ejection fraction. A stipulated chamber changing from $200$ to $150\mathrm{mL}$ ejects $50\mathrm{mL}$ with EF $25\%$. Another changing from $120$ to $60\mathrm{mL}$ ejects $60\mathrm{mL}$ with EF $50\%$. A larger filled volume need not produce a larger stroke volume. These are constructed mechanical examples, not diagnostic cutoffs or reference ranges.

Imaging can test several parts of this mechanism. Echocardiography follows chamber dimensions and contraction; cine magnetic resonance imaging can quantify volumes and longitudinal motion. In a primary study, Marcus Carlsson and colleagues compared twelve patients with dilated cardiomyopathy, twelve controls and twelve elite triathletes. Their analysis combined atrioventricular-plane displacement with anatomical area to investigate the longitudinal contribution to ventricular pumping.^[ref]

This experiment illustrates why the condition cannot be represented by one chamber diameter alone: geometry, motion and transported volume supply different information. Doppler echocardiography and its velocity-time integral provide complementary flow observations, while a clinical diagnosis also requires the surrounding evidence and cause of the myocardial abnormality.

Doppler echocardiography combines echocardiography with Doppler ultrasound to examine motion, particularly blood flow, in and around the heart. The image locates anatomical structures, while frequency shifts in returning ultrasound provide information about motion along the beam. It supplies a velocity measurement rather than a direct measurement of cardiac output.

For a moving scatterer with speed $v$, beam-to-flow angle $\theta$, transmitted frequency $f_0$ and sound speed $c$, the leading approximation isThe two-way factor arises because the outgoing and returning wave both interact with the moving scatterer. For stipulated $f_0=2.5\mathrm{MHz}$, $v=1.0m/s$, $c=1540m/s$ and $\theta =0$, the shift is about $3.25\mathrm{kHz}$. At $60^{\circ }$ the same flow gives half that shift. Interpreting the latter as perfectly aligned flow would underestimate the speed by a factor of two.

Pulsed-wave Doppler echocardiography uses timing to select a sampling region, whereas continuous-wave Doppler echocardiography receives signals continuously along the beam. The acquired velocity spectrum and the selected anatomical region must therefore be interpreted together. A moving tissue signal and a blood-flow signal are different observations even if both produce a Doppler effect.

A motivating primary validation by Halfdan Ihlen and colleagues compared Doppler-derived cardiac output with independent thermodilution and Fick measurements. The protocol included changes in flow during dobutamine infusion, testing correspondence over changing conditions rather than only one resting observation.^[ref]

Turning a velocity record into transported volume additionally requires an appropriate flow area and representative velocity distribution. The velocity-time integral makes that connection explicit. A large peak velocity alone neither determines the volume moved per beat nor identifies a unique clinical diagnosis.

Echocardiography uses ultrasonography to form moving images of the heart. Returning sound waves reveal the dimensions and motion of its chambers and heart valves, making structure and pumping visible during the same examination.

In the common transthoracic approach, an acoustic transducer transmits pulses through the chest and receives reflected signals. A computer reconstructs their spatial and temporal pattern into images. The resulting measurements contribute to clinical diagnosis alongside the clinical history and other observations; an image and its interpretation are distinct stages of the assessment.^[ref]

Inflammation of the inner lining of the heart, often involving valves. Infective endocarditis is the microbial form; the broader anatomical term does not itself establish infection.

The inner endothelial lining of the heart, which also provides developmental signals to neighbouring myocardium.

Coauthor of research on the transient regenerative capacity of the neonatal mouse heart. The study connected age with recovery after injury, showing why regenerative behavior cannot be assumed constant across development.^[ref]