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Case report no. 1,
Department Pathological Physiology
V. Danzig, MD, PhD,
2nd Dept. Internal Medicine
Cardiology and Angiology Division
1st Med.F CUNI
Patient history
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78 yr. old male, retiree, worked as mechanical engineer
Family history: longevity, cardiovascular complications,
yet no early deaths
(Ab)usus: quitted smoking 15 yrs ago, 10-15 cigarettes
daily before, alcohol drinking denies
Patient history: repeated herniotomy, benign prostatic
hypetrophy, diabetes mellitus last 6 years – on diet
Patient history - questions
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What is the risk (high/ medium/ low) of cardiovascular
disease in this 78 year old former smoker?
When is the onset of cardiovascular disorder
considered early and when timely?
What are the effects of smoking on the cardiovascular
system and on the respiratory system (related to
malignant tumors), what are the differences?
Current disorder
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Last 3 years progression of exertional dyspnea and
chest pain projecting to medium and lower sternum
Progressive worsening last 2 weeks, pains in rest
Once a pain attack in walking, loss of consciousness,
awakened lying on ground
Admitted to hospital after a nigh long lasting retrosternal pains, dyspnea, felt forced to sit, first time felt as
well irregular and fast heardbeats
Current disorder - questions
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Give clinical definition of dyspnea. What is its origin in (left)
heart disorder? Other causes besides cardiomyopathy?
Name/ description: ischemic myocardial pain, its
mechanism/ cause?
Name/ description: of a short time loss of consciousness
What is the prime cause of myocardial ischemia in Czech
population? What is differential diagnostics?
Synonyms for palpitations? They are signs of what
diseases? What does it mean when patient complains that
they are irregular?
What investigation methods to use in this patient
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ECG: - what are signs of acute myocardial infarction?
Elevations of the ST segment?
- cardiac rhythm ?
Biochemical markers – in this patient were not elevated
– no myocardial necrosis
X-ray of heart and lungs – venostasis (oedema)
ECG at admission
Next: atrial fibrillation w. wide QRS complexes
Definition of atrial fibrillation
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Atrial fibrillation is an irregular atrial activity. ECG record
shows no P waves. Instead there are fast oscillations,
also denoted as “F” waves. Ventricular response are
typically QRS complexes with RR intervals of different
length.
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Investigation methods - questions
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How many leads are in standard ECG? Names and
groups of leads? How we record continuous ECG and
how many leads in it we use?
Name biochemical cardiac markers, describe them,
what is their use?
What are signs of atrial fibrillation? What are the risks?
Further investigations
• echokardiography, ECHO:
- Findings: calcified aortal valve with limited cusp
excursions, Doppler – tight stenosis w. gradients 65/ 34
mm Hg, mouth area 0.4 cm2/m2 (per body surface)
- Ascendent aorta dilation
- dilatace ascendentní aorty
- EF (ejection fraction) LV 0,45 – 0,49 (= 45-49%)
• selective coronarography: no pathology/ normal findings
ECHO – morphological investigation
ECHO – continuous Doppler
Cathetrisation record – aortal stenosis
Further investigations - questions
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What gradient is important here (related to aortal valve
and its stenosis)
What are two basic approaches to measure the
gradient? Compare the two? Can we always use both of
them?
What can be the complications?
Why we calculate the area? Explain cases when area is
significantly reduced yet the high gradient is not
present.
What is left ventricle ejection fraction, its units and
normal values?
Therapy
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Temporary therapy: aim to compensate – therapy of
heart failure and control of ventricular response to atrial
fibrillation
Definitive therapy: replacement of aortal valve by bioprosthesis, eventually a plastic surgery of ascendent
aorta
Therapy - questions
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What is the relation of atrial fibrillation to the principal
heart disorder (aortal stenosis)?
Why as a first step in the therapy of atrial fibrillation we
need a slow down of the ventricular frequency?
Why and when a plastic surgery of aorta is needed as
well?
Conclusions I
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Aortal stenosis: is frequent and becoming yet more
frequent acquired valve disorder, as the population is
ageing.
This condition is followed up by a pressure overload of
left ventricle. This propagates backwards and leads to
atrial dilation (closing a vicious circle this way) and back
to pulmonary circulation.
Typical compensatory mechanism is left ventricle
hypertrophy. This is followed up by development of
ventricle dilation, deterioration of systolic function and
failure.
Conclusions II
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Symptomes and their patho-physiological explanations (Q/+A):
dyspnoe
- by back-propagation of elevated intra-ventricular pressure
- stenocardia
- lowered throughput in coronary arteries, esp. in tachycardia
- exertional syncope
- inability to elevate cardiac output when valve mouth area is reduced
- low pressure amplitude
- slower onset of systolic pressure in aorta
• Therapy: aortal valve replacement (bio-prosthesis) by cardio-surgery.
Transcatheter Aortic Valve Implantation in selected high risk patients.