CVS:
Keyword (s) Condition Associated
Squatting position, +ve Schamroth sign Tetralogy of Fallot
(clubbing) (Remember: Squatting; in cases of tetralogy of
Fallot -> reduces the resistance and thus
increases pulmonary blood flow -> thus
reducing signs of cyanosis)
“Aschoff” bodies Acute stage of Rheumatic fever
(microscopic feature)
“Fish” mouth Fibrosing stage of Rheumatic fever
(macroscopic feature)
Also seen rheumatic fever endocarditis -
e.g. in the MV
“Sea anemone” appearance Papillary fibroblastoma (fibrosing stage of
Rheumatic fever; microscopic feature)
Dimpled raphe Bicuspid aortic stenosis
Fusion of commissures + presence of Rheumatic aortic stenosis
triangular orifice (AV)
Myxoid stroma “plastered” onto the aortic AV insufficiency, also characteristic sign of
side of the cusps the usage of fen-phen drug
Tips of papillary muscle insertion is “pearly Tricuspid valve (TV) stenosis
white” (TV)
Pt use drug fen-phen MV insufficiency, AV insufficiency
(NOTE: Glistening appearance as well is
noted on valves of pts taking fen-phen drug;
anti-migraine drug)
“Pitting” oedema Right-sided HF
(Remember: RHF -> thus not enough blood
going to the lungs to pick up O2 -> thus renal
hypoxia -> thus the fluid remains in the
periphery causing fluid retention and oedema ->
“pitting” oedema, ascites etc.)
“Aschoff nodules” = “Anitschkow myocytes” Rheumatic fever endocarditis
+ “Aschoff cells”
Group A β haemolytic streptococcus Rheumatic fever
pyogenes
“Granulomatous stage” of “Aschoff nodules” Rheumatic fever (endocarditis)
(develops 1-2 months after onset of clinical
symptoms, develops within/near foci of fibrinoid
necrosis -> replaced collagen scar tissue)
MacCallum plaque Rheumatic fever endocarditis
(Reminder: L side is more affected than the R
, side; MV and AV > TV and PV)
Migratory polyarthritis, increased ESR Acute RF (non-cardiac symptoms and
(Erythrocyte sedimentation Rate), arthritis, signs)
fever, malaise, arthralgia, skin (erythema
marginatum), CNS (Sydenham chorea)
Staphylococcus aureus Acute infective endocarditis
Streptococcus viridans Subacute infective endocarditis
Endocarditis that affects the right-sided Endocarditis of the carcinoid syndrome
valves; left-sided are rarely involved (Remember: since blood from the GI carcinoids
will enter via the right side of the heart, thus the
right-sided valves will be bathed with the
released mediators; VAPs and amines, of the
carcinoid tumours)
“Spider cells” Rhabdomyoma (Microscopic features)
(Remember: it’s common in children)
“Lepidic” cells Myxoma
“Crescendo” Unstable angina
ST segment elevation, pathological Q wave STEMI
(sometimes T wave inversion is present, but it is
not specific to STEMI)
ST depression and/or T wave inversion NSTEMI
“Stiff heart syndrome” Restrictive cardiomyopathy
(cardiac amyloidosis)
Cardiomyopathy that would be found in a Hypertrophic cardiomyopathy
young, athletic patient (thickened LV)
Naxos syndrome Arrythmogenic Right Ventricular
cardiomyopathy
“Bare nuclei” Myocarditis
“Bread and Butter” Fibrinous or sero-fibrinous pericarditis
, “Scintillating (sparkling) gold pain Idiopathic cholesterol pericarditis
appearance”
Pericarditis that is characterised by the Purulent pericarditis
present of yellowish/cloudy exudate
“Pipe-stem” arteries Moenckeberg arteriosclerosis (Medial
Calcific Sclerosis)
“Glass-like” appearance, “benign Hyaline arteriolosclerosis
nephrosclerosis” (Remember: benign nephrosclerosis is due to
long standing hypertension)
“Onion-skin” appearance Hyperplastic arteriolosclerosis
“Malignant nephrosclerosis” Hyperplastic arterioloscerlosis (because of
malignant hypertension)
“Type A” personality Atherosclerosis (risk factor of developing
atherosclerosis)
“Vulnerable” plaque Unstable atheroslerotic plaque
(Remember: inflammatory cells > smooth
muscle cells, and since there is a greater
amount of inflammatory cells thus there is a
thinner fibrous ap -> acute rupture -> leads to
thrombosis and/or embolism. Also since the lipid
component is greater compared to a stable
plaque -> thus making this plaque unstable)
Loose platelet plaque Haemostasis (pathogenesis)
Cystic Medial necrosis/degeneration Marfan syndrome
Dissection of the proximal ascending Marfan syndrome
thoracic aorta
“Tree-bark” appearance Syphilitic (luetic) aneurysm
Keyword (s) Condition Associated
Squatting position, +ve Schamroth sign Tetralogy of Fallot
(clubbing) (Remember: Squatting; in cases of tetralogy of
Fallot -> reduces the resistance and thus
increases pulmonary blood flow -> thus
reducing signs of cyanosis)
“Aschoff” bodies Acute stage of Rheumatic fever
(microscopic feature)
“Fish” mouth Fibrosing stage of Rheumatic fever
(macroscopic feature)
Also seen rheumatic fever endocarditis -
e.g. in the MV
“Sea anemone” appearance Papillary fibroblastoma (fibrosing stage of
Rheumatic fever; microscopic feature)
Dimpled raphe Bicuspid aortic stenosis
Fusion of commissures + presence of Rheumatic aortic stenosis
triangular orifice (AV)
Myxoid stroma “plastered” onto the aortic AV insufficiency, also characteristic sign of
side of the cusps the usage of fen-phen drug
Tips of papillary muscle insertion is “pearly Tricuspid valve (TV) stenosis
white” (TV)
Pt use drug fen-phen MV insufficiency, AV insufficiency
(NOTE: Glistening appearance as well is
noted on valves of pts taking fen-phen drug;
anti-migraine drug)
“Pitting” oedema Right-sided HF
(Remember: RHF -> thus not enough blood
going to the lungs to pick up O2 -> thus renal
hypoxia -> thus the fluid remains in the
periphery causing fluid retention and oedema ->
“pitting” oedema, ascites etc.)
“Aschoff nodules” = “Anitschkow myocytes” Rheumatic fever endocarditis
+ “Aschoff cells”
Group A β haemolytic streptococcus Rheumatic fever
pyogenes
“Granulomatous stage” of “Aschoff nodules” Rheumatic fever (endocarditis)
(develops 1-2 months after onset of clinical
symptoms, develops within/near foci of fibrinoid
necrosis -> replaced collagen scar tissue)
MacCallum plaque Rheumatic fever endocarditis
(Reminder: L side is more affected than the R
, side; MV and AV > TV and PV)
Migratory polyarthritis, increased ESR Acute RF (non-cardiac symptoms and
(Erythrocyte sedimentation Rate), arthritis, signs)
fever, malaise, arthralgia, skin (erythema
marginatum), CNS (Sydenham chorea)
Staphylococcus aureus Acute infective endocarditis
Streptococcus viridans Subacute infective endocarditis
Endocarditis that affects the right-sided Endocarditis of the carcinoid syndrome
valves; left-sided are rarely involved (Remember: since blood from the GI carcinoids
will enter via the right side of the heart, thus the
right-sided valves will be bathed with the
released mediators; VAPs and amines, of the
carcinoid tumours)
“Spider cells” Rhabdomyoma (Microscopic features)
(Remember: it’s common in children)
“Lepidic” cells Myxoma
“Crescendo” Unstable angina
ST segment elevation, pathological Q wave STEMI
(sometimes T wave inversion is present, but it is
not specific to STEMI)
ST depression and/or T wave inversion NSTEMI
“Stiff heart syndrome” Restrictive cardiomyopathy
(cardiac amyloidosis)
Cardiomyopathy that would be found in a Hypertrophic cardiomyopathy
young, athletic patient (thickened LV)
Naxos syndrome Arrythmogenic Right Ventricular
cardiomyopathy
“Bare nuclei” Myocarditis
“Bread and Butter” Fibrinous or sero-fibrinous pericarditis
, “Scintillating (sparkling) gold pain Idiopathic cholesterol pericarditis
appearance”
Pericarditis that is characterised by the Purulent pericarditis
present of yellowish/cloudy exudate
“Pipe-stem” arteries Moenckeberg arteriosclerosis (Medial
Calcific Sclerosis)
“Glass-like” appearance, “benign Hyaline arteriolosclerosis
nephrosclerosis” (Remember: benign nephrosclerosis is due to
long standing hypertension)
“Onion-skin” appearance Hyperplastic arteriolosclerosis
“Malignant nephrosclerosis” Hyperplastic arterioloscerlosis (because of
malignant hypertension)
“Type A” personality Atherosclerosis (risk factor of developing
atherosclerosis)
“Vulnerable” plaque Unstable atheroslerotic plaque
(Remember: inflammatory cells > smooth
muscle cells, and since there is a greater
amount of inflammatory cells thus there is a
thinner fibrous ap -> acute rupture -> leads to
thrombosis and/or embolism. Also since the lipid
component is greater compared to a stable
plaque -> thus making this plaque unstable)
Loose platelet plaque Haemostasis (pathogenesis)
Cystic Medial necrosis/degeneration Marfan syndrome
Dissection of the proximal ascending Marfan syndrome
thoracic aorta
“Tree-bark” appearance Syphilitic (luetic) aneurysm
