Download Diastolic mitral regurgitation: a borderline case in cardiovascular

European Review for Medical and Pharmacological Sciences
2003; 7: 161-170
Diastolic mitral regurgitation: a borderline
case in cardiovascular physiology
N. ALESSANDRI, S. MARIANI, F.R. MESSINA, G. RONDONI, E. GERBASI,
L. BATTISTA, C. GAUDIO
Dipartimento Scienze Cardiovascolari e Respiratorie,
University of Rome “La Sapienza” – Rome (Italy)
Abstract. – Background: Mitral regurgitation during diastole in 5 subjects, of whom 4 affected by cardiovascular disease and 1 healthy
competitive athlete, was the aim of this work.
The 4 patients are respectively affected by:
1rst case: arterial hypertension, dyslipidemia and
III degree AV block in NYHA class II heart failure
(HF); 2nd case: NYHA III HF, prosthetic biologic
aortic valve dysfunction; 3th case: NYHA III HF,
ischemic dilated cardiomyopathy; 4th case: ischemic dilated cardiomyopathy waiting for heart
transplantation.
Methods and Results: The above 4 patients
showed, on transthoracic echocardiogram, mitral diastolic regurgitation. The authors deem as
caused, in agreement with the literature, both by
an atrio-ventricular pressure gradient inversion
during long-lasting diastoles (III degree atrioventricular block, blocked atrial systole, aortic
valve regurgitation), and by an inadequate ventricular remodelling/distensibility.
The 5th case deals with a healthy highly
trained competitive athlete who, at the fitness
checkup, showed mitral diastolic regurgitation.
The study was also extended to two healthy
groups of subjects, in order to rule out mitral regurgitation during the diastolic interval of the
cardiac cycle.
Conclusions: Such finding, after an accurate
and critical analysis, led the authors to assume
it may deal with a borderline physiological condition.
Key Words:
Cardiovascular physiology; Mitral valve; Regurgitation.
Introduction
Cardiac cycle, described by the electro-mechanical-hemodynamic diagram by Wiggers1-3,
lasts 800 msec at a heart rate (HR) of 60
beats/min and is composed by successive
phases which illustrate cardiocirculatory dynamics.
Atrial contraction (100 msec) relates to the
P wave on surface electrocardiogram (ECG),
and contributes to 15-20% of ventricular diastolic blood volume4-8.
After the Q wave, ventricular systole (270
msec) begins marked by three intervals: (1)
Isovolumetric contraction (50 msec); (2)
Rapid ejection: lasts 1/3 of the whole ejection
time; (3) Slow ejection: 2/3 of the whole ejection and varies with HR.
After the T wave, ventricular diastole begins (530 msec) marked, according to
Brutsaert9-12, by four lapses: (1) Isovolumetric
relaxation (80 msec); (2) Rapid filling (100
msec): 75-80% of diastolic blood volume inflows; (3) Slow filling (220 msec and changes
with HR) contributes to 10-15% of blood
volume; (4) Atrial systole (100 msec) which
contributes to 15-20% of diastolic blood volume.
Ventricular diastole is made up of: (1) an
active phase 13-16 (isovolumetric relaxation
and rapid filling) during which heart muscle
goes back to resting conditions; (2) a passive
phase (slow filling) during which myocardial
compliance (or elasticity/stiffness) conditions
ventricular filling11,12.
Myocardial stiffness is subdivided into:
(1) “Wall stiffness”: pressure change divided
by volume change (dP/dV); (2) “Chamber
stiffness”: represents resistance to myocardial stretching (force per surface unit) in relation to a tension (length change per length
unit13-19.
Several factors contribute to determine
ventricular pressure/volume curve during di161
N. Alessandri, S. Mariani, F.R. Messina, G. Rondoni, E. Gerbasi, L. Battista, C. Gaudio
astole. Relaxation velocity and diastolic suction prevail in the early phase of diastole;
pericardial status, pulmonary engorgement
and coronary engorgement contribute to
myocardial stiffness/elasticity in late
diastole13-16; 20-23.
The heart is continuously liable to a series
of autonomic and neurohormonal stimuli, in
order to warrant an output meeting body
needs24-33. Heart cycle duration/velocity is influenced by different factors, such as: HR,
left atrial pressure, diastolic ventricular pressure, pulmonary arteries to capillaries gradient, cardiac rhythm, atrio-ventricular conduction34-38.
We have found out a backflow (from ventricles to atria) through the atrioventricular
valves, during mid-end-diastole, in four patients (pts) affected by left ventricular failure
and in a highly trained athete15,16,20.
We wanted to study the meaning of this
flow in relation to the heart cycle dynamics,
particularly diastolic phase oriented. Is this
flow an expression of ventricular physiopathology or can it be considered as an extreme physiologic condition?
For the sake of scientific methodology 2
groups have been included (group A and
group B) respectively made up of 20 soldiers
and 16 highly trained competitive athles, in
order to screen normal physiologic conditions.
Group A (Gr. A) was made up of operative recruited military men, average age 20.9
± 0.8 (range 20-22), with body surface 1.84 ±
0.08 m2.
Group B (Gr. B) was made up of 16 male
marathon-runner highly trained competitive
athletes, average age 49.9 ± 8.2 (range 42-66),
with body surface 1.77 ± 0.1 m2.
Blood pressure was taken, and average and
differential pressures were calculated on inclusion; a color-Doppler TTE by an ATL
echocardiomachine, with a 2.5 MHz probe
was carried out. As for the latter, standard
views and measures were taken according to
criteria of the American Society of
Echocardiography43. Continuous and pulsed
wave Doppler examination, for the study of
transvalvular flow, was performed from the
apical view, avoiding any possible technical
mistake in flow detection (aliasing in particular).
Materials and Methods
Five out of 15,000 subjects undergoing a
transthoracic echocardiogram in our outpatient ward, since 1998 to 2003, have been
studied.
Such subjects were all male, average age
48.4 ± 7.56, of whom 4 affected by heart disease and 1 in good health.
Inclusion was done detecting a backflow
from the left ventricle toward the left atrium
during ventricular diastole, by transthoracic
echo-Doppler examination (TTE), interpreted as mitral diastolic regurgitation39-42.
The 4 heart-diseased patients’ cardiovascular data were derived from clinical charts;
blood tests, ECG dynamic monitoring, myocardial scanning (basal and after dipiridamole), cardiac catheterization and selective
coronary angiograms had been carried out.
The athlete’s data were derived from the
yearly fitness medical chart: blood tests, ECG
dynamic monitoring, exercise ECG stress
test, basal and stress TTE, autonomic screening test.
162
Analysis Mode
We estimated: enddiastolic (EDD) and
endsystolic (ESD) diameters, left ventricular
enddiastolic (EDLVV) and endsystolic volume (ESLVV) by Teichholz’s and Simpson’s
formula, interventricular septum (SWT) and
posterior wall thickness (PWT), left atrial
transverse diameter (LA), ventricular ejection fraction (EF) and shortening fraction
(SF); myocardial mass according to Penn’s
criteria, endsystolic wall stress according to
Wilson’s formula, average systolic wall stress
according to Quinone’s formula, beta-stiffness and wall distensibility, left ventricular
strain.
Transvalvular and and pulmonary venous
flows were Doppler-estimated.
Maximum protodiastolic (Vmax E) and enddiastolic (Vmax A)11,39 velocity, protodiastolic
(Area E) and enddiastolic (Area A) spectral
area, protodiastolic flow deceleration time,
protodiastolic flow pressure half-time (PHT)
and isovolumetric relaxation time were estimated as for mitral flow.
Diastolic mitral regurgitation: a borderline case in cardiovascular physiology
Systolic flow maximum velocity (V max J)
and its spectral area (Area J), diastolic flow
maximum velocity (Vmax K) and its spectral
area (Area K), atrial backflow maximum velocity (V max AR) and spectral area (Area
AR) were estimated as for pulmonary venous
flow.
In the data statistical processing the average and standard deviations were calculated.
All data were PC tabbed and processed by
a statistical program (Microsoft Excel).
Cases Description
1rst case: 39 years old man, with sedentary
job (switchboard operator), with diabetes II
for over 20 years, hypertension-treated for
over 10 years (last treatment: ACE-inhibitor, calcium-antagonist, antiplatelet
drug), no dyslipidemia; at the outpatient
checkup he reports a lypothymic event, ef-
fort dyspnea, palpitation, no vision blurring,
no angina; class II NYHA; blood pressure
140/90 mm Hg; ECG: III degree atrio-ventricular (AV) block, with junctional escape
rhythm 55/m’ and aspecific changes of ventricular repolarization. He is admitted for
pacemaker implantation. Holter monitoring: constant III degree AV block throughout 24 hours with 70/m’ mean sinus rate and
40/m’ mean ventricular rate. Rare monofocal ventricular ectopic beats (VEB) (Lown I
B). No other noteworthy disease (Tables I,
II, III).
2nd case: 60 years old man hospitalized in
the heart surgery ward, in class III NYHA
heart failure, because of prosthetic biologic
aortic valve dysfunction39,44.
Operated in 1989, he is admitted because
of slight effort dyspnea, asthenia, palpitation,
nicturia. TTE: severe prosthetic valve regurgitation and slight stenosis; ECG: sinus
rhythm with left ventricular overload (Tables
I, II, III).
Table I. Clinical and echocardiografic parameters.
Age
BS
HR
SBP
DBP
ABP
DBP
DE
EF
DSWT
SSWT
DPWT
SPWT
EDVD
ESVD
EDVD/ESVD
SF
EDLVV(TEICH)
ESLVV(TEICH)
EDLVV(SIMP)
ESLVV(SIMP)
EF(SIMP)
EF(TEICH)
1rst case
2nd case
3th case
4th case
5th case
39
1.83
40
150
90
110.0
60
22.5
92.77
9.2
14
9.2
14.3
53.8
36.7
17.1
31.78
140.1
49.7
146.4
37
74.73
64.53
60
1.72
68
130
40
70.0
90
23.5
126.42
12
14
12
15
84
61
23
27.38
384.2
286.9
405.6
282.2
30.42
25.33
54
1.91
100
105
85
91.67
20
21.4
132
9.6
13.6
10
14
87.7
73.8
13.9
15.85
462.7
327.7
498.3
341.4
31.49
29.18
44
1.77
95
110
85
93.33
25
20
119.2
8.3
13.2
8.5
13.2
90.5
82
8.5
9.39
525.7
384.3
570.1
410.3
28.03
26.90
45
1.84
50
135
85
101.67
50
27.7
126.42
8.5
14.2
9.6
15.4
59.8
39.8
20
33.55
179.26
71.33
167.7
59.7
64.40
60.21
BS = body surface; HR = heart rate; SBP = systolic blood pressure; DBP = diastolic blood pressure; ABP = average
blood pressure; DBP = differential blood pressure; EF = ventricular ejection fraction; DSWT = diastolic septum wall
thickness; SSWT = systolic septum wall thickness; DPWT = diastolic posterior wall thickness; EDVD = enddiastolic
ventricular diameter; ESVD = endsystolic ventricular diameter; SF = shortening fraction; EDLVV = enddiastolic left
ventricular volume; ESLVV = endsystolic left ventricular volume; TEICH = Teichholz’s; SIMP = Simpson’s.
163
N. Alessandri, S. Mariani, F.R. Messina, G. Rondoni, E. Gerbasi, L. Battista, C. Gaudio
Table II. Echocardiografic parameters cardiac and aortic function evaluation.
LVM
LVM/BS
LVM/EDLVV
LVHD
LVHD/BS
ContrTEICH
ContrSIMP
DWS
SWS
Vmax E (MF)
Vmax A (MF)
Vmax E/Vmax A
Vmax J (PVF)
Vmax K (PVF)
Vmax AR (PVF)
DT
IVRT
AC
AS
βS
EM
EM2
1rst case
2nd case
3th case
4th case
5th case
241.34
131.88
1.64
1.46
0.79
3.018
4.05
123.06
258.71
95
40
2.37
40
45
38
246.97
77.15
11.68
26.59
2.09
2.28
0.85
736.29
428.07
1.81
1.75
1.01
0.453
0.46
188.49
363.68
79
70
1.12
54
30
32
425.83
159.69
6.30
27.70
3.12
2.38
1.58
643.42
336.87
1.29
2.23
1.17
0.320
0.30
206.67
373.41
110
60
1.83
52
40
35
198.88
150.92
14.16
18.83
1.92
1.96
0.70
569.40
321.69
0.99
2.69
1.52
0.286
0.26
261.46
454.41
100
30
3.33
48
36
33
218.81
172.82
6.23
10.36
2.48
2.41
1.60
306.31
166.47
1.82
1.65
0.89
1.892
2.26
111.74
241.42
52
39
1.33
32
50
25
127.80
27.39
15.11
50.25
0.92
0.99
0.66
LVM = left ventricular mass; BS = body surface; EDLVV = enddiastolic left ventricular volume; LVHD = left ventricular hypertrophy degree; Contr = contractility; TEICH = Teichholz’s; SIMP = Simpson’s; DWS = diastolic wall
stress; SWS = systolic wall stress; Vmax E= maximum protodiastolic velocity; Vmax A = maximum end diastolic velocity;
MF = mitral flow; PVF = pulmonary venous flow; DT = deceleration time; IVRT = isovolumetric relaxation time; AC
= aortic compliance; AS = aortic strain; βS = β-stiffness; EM = elasticity modulus.
3 th case: 54 year old man affected by ischemic dilated cardiomyopathy, in class III
NYHA heart failure with EF = 30%; ECG:
sinus rhythm, V1 to V5 QS waves, low peripheral QRS voltage. Hypertensive, dyslipidemic, heavy smoker.
First hospitalization in 1987 due to anterolateral acute myocardial infarction
(AMI), second one in 1994 due to A inferior
AMI. Sudden cardiac death in 2001 (Tables
I, II, III).
4th case: 44 years old man, married, bankclerk, no job in last 6 months; first hospitalization in 1990 for anterior AMI, second hospitalization in 1998 for inferoposterior AMI. At
Table III. Patients clinical characteristics.
Patients
1rst case
2nd case
3th case
4th case
5th case
Age
BS
Disease
MI
AI
TI
LV/A grad
BEM
39
1.83
III degr AVB
1°
–
–
–
–
60
1.72
PBAoV disfunction
1°-2°
3°
1°
45 mmHg
I.C.
54
1.91
DM
2°
1°
1°-2°
No
I.C.
44
1.77
DM
2°-3°
1°
2°
No
I.C.
45
1.84
–
–
–
0.5
–
–
LVM = left ventricular mass; BS = body surface; EDLVV = enddiastolic left ventricular volume; LVHD = left ventricular hypertrophy degree; Contr = contractility; TEICH = Teichholz’s; SIMP = Simpson’s; DWS = diastolic wall
stress; SWS = systolic wall stress; Vmax E= maximum protodiastolic velocity; Vmax A = maximum end diastolic velocity;
MF = mitral flow; PVF = pulmonary venous flow; DT = deceleration time; IVRT = isovolumetric relaxation time; AC
= aortic compliance; AS = aortic strain; βS = β-stiffness; EM = elasticity modulus.
164
Diastolic mitral regurgitation: a borderline case in cardiovascular physiology
present ischemic dilated cardiomyopathy, in
class III NYHA failure, waiting for heart transplantation; EF = 22%; ECG: sinus rhythm,
right bundle branch block (RBBB) + left anterior hemiblock (LAH) (Tables I, II, III).
5th case: 45 years old man, no heart disease,
no dyslipidemia, no diabetes. He served in
the army. Fit for sports competitive activity.
Normal job (lawyer). Married, with two children in good health. No cardiovascular nor
neoplastic familiarity. Usual rash diseases
during childhood. Appendicectomy at 22
years. Sports training for over 26 years, competitive one during the last 18 years.
Marathon-runner with 26 hours and minimal
70 km run, weekly training. Competition time
between 2.40 and 2.55 hours in the 42 km
classic race. He undergoes regular medical
checkups and yearly a sports fitness polispecialty medical appraisal. Blood pressure
120/70 mmHg. Holter ECG with tracings and
trends within normal limits. Ergometric test:
no effort induced myocardial ischemia.
Normal tilt test (Tables I, II, III).
Gr. A: 20 healthy soldiers, with the same
medical profile, belonging to the same operative group, employed for 305 ± 10 days, not
taking any drug for over 1 year.
Laboratory tests all within normal range
(Tables IA, IIA, IIIA)
Gr. B: 16 competitive athletes who had
been training for over 15 years (average 18 ±
1.6), with 30-35 weekly training hours and a
minimal 70 km running, competition times
ranging from 2 hours and 40 min to 2 hours
and 55 min in the 42 Km and 55 mt
marathon-running. They all were healthy and
had not been taking drugs for over 1 year.
Lab tests all within normal range (Tables IA,
IIA, IIIA).
No diastolic flow at the atrio-ventricular
valves, from ventricle to atrium, was found
either in Gr. A or in Gr. B45.
Results
For each patient, all parameters taken in
the various instrumental examinations are
reported and processed in Tables I, II and
III. Figures 1 and 2 show pulsed-wave
Doppler with transvalvular mitral flow taken from the apical view. We find out, during
long diastoles or after a blocked P wave on
the surface ECG, the occurrence of a transvalvular regurgitant flow. This finding
means a diastolic regurgitation into the left
atrium.
Case 1: III degree AV block, diabetes, hypertension, abnormal morphologic and hemodinamic data; feature in agreement with diastolic ventricular dysfunction; bioptic-histologic appraisal lacks for complete study. As literature-reported20,48 the abnormal slow rythm
helped in worsening ventricular compliance.
Cases 2, 3, 4: The outcome of instrumental
examinations is completely abnormal, showing a systo-diastolic myocardial derangement
and is in agreement with each patient’s NYHA class.
Table IA. Clinical and echocardiografic parameters.
N° tot.
Age
BS
HR
SBP
DBP
ABP
DBP
DEmitral
EFmitral
DSWT
SSWT
DPWT
SPWT
EDVD
ESVD
S.F.
EDLVV(TEICH)
ESLVV(TEICH)
EDLVV(SIMP)
ESLVV(SIMP)
EF(SIMP)
EF(TEICH)
Gr. A
Gr. B
20
20.87 ± 0.78
1.84 ± 0.08
74.7 ± 13.7
126.2 ± 13.5
78.1 ± 5.5
94.2 ± 7.1
48.1 ± 11.7
21.2 ± 2.4
115.8 ± 23.6
8.7 ± 0.5
12.1 ± 1
8.5 ± 0.7
13.5 ± 1.3
48 ± 3.9
30.6 ± 3.8
38 ± 4.8
109.06 ± 20.7
36.2 ± 10.4
92.9 ± 22.6
30.3 ± 11.7
71.4 ± 6.2±
67.3 ± 6.5
16
49.9 ± 7.8
1.77 ± 0.1
54.3 ± 6.9
137.5 ± 9.2
86.4 ± 6.1
103.4 ± 6
51.07 ± 8.6
22.7 ± 2.2
117.07 ± 18.9
8.7 ± 1.5
14 ± 2.1
8.8 ± 1.6
15.2 ± 2.6
60.4 ± 4.8
36.4 ± 4.4
39.5 ± 5.3
183.3 ± 32
59.2 ± 17.7
166.4 ± 46.6
51.2 ± 16.6
67.3 ± 5.7
69.4 ± 7.2
BS = body surface; HR = heart rate; SBP = systolic
blood pressure; DBP = diastolic blood pressure; ABP =
average blood pressure; DBP = differential blood pressure; EF = ventricular ejection fraction; DSWT = diastolic septum wall thickness; SSWT = systolic septum
wall thickness; DPWT = diastolic posterior wall thickness; EDVD = enddiastolic ventricular diameter; ESVD = endsystolic ventricular diameter; SF = shortening
fraction; EDLVV = enddiastolic left ventricular volume; ESLVV = endsystolic left ventricular volume; TEICH = Teichholz’s; SIMP = Simpson’s.
165
N. Alessandri, S. Mariani, F.R. Messina, G. Rondoni, E. Gerbasi, L. Battista, C. Gaudio
Table IIA. Echocardiografic parameters, r cardiac and
aortic function evaluation.
LVM
LVM/BS
LVM/EDLVV
LVHD
LVHD/BS
ContrTEICH
ContrSimp
DWS
SWS
Vmax E (MF)
Vmax A (MF)
Vmax E/Vmax A
Vmax J (PVF)
Vmax K (PVF)
Vmax AR (PVF)
DT
IVRT
AC
AS
bS
EM
EM2
Gr. A
Gr. B
181.23 ± 19.7
98.43 ± 12.8
2.02 ± 0.3
1.39 ± 0.18
0.75 ± 0.1
3.9 ± 1.5
4.8 ± 2
196.9 ± 25.3
86.6 ± 16.9
89 ± 20.4
56.9 ± 15.5
1.6 ± 0.3
53 ± 2.5
62.3 ± 6.1
17.5 ± 2.7
135 ± 15.6
61 ± 8
6.28 ± 2.3
18.4 ± 2.8
2.7 ± 0.95
1.83 ± 0.67
2.7 ± 0.5
285.09 ± 73.4
160 ± 38.4
1.79 ± 0.5
1.76 ± 0.32
0.99 ± 0.19
2.5 ± 0.8
2.6 ± 0.7
232.2 ± 53.35
106.67 ± 31.3
68.2 ± 13
56.3 ± 11.6
1.23 ± 0.2
55.07 ± 15.7
46.8 ± 9.73
26.1 ± 7.4
143 ± 18.6
65.4 ± 5.8
4.6 ± 1.7
15.4 ± 5.6
3.4 ± 1.2
3.7 ± 1.3
2.5 ± 0.9
LVM = left ventricular mass; BS = body surface;
EDLVV = enddiastolic left ventricular volume; LVHD
= left ventricular hypertrophy degree; Contr = contractility; TEICH = Teichholz’s; SIMP = Simpson’s; DWS =
diastolic wall stress; SWS = systolic wall stress; Vmax E =
maximum protodiastolic velocity; Vmax A = maximum
end diastolic velocity; MF = mitral flow; PVF = pulmonary venous flow; DT = deceleration time; IVRT =
isovolumetric relaxation time; AC = aortic compliance;
AS = Aortic strain; βS = β-stiffness; EM = elasticity
modulus.
Figure 1.
Case 5: No detectable left ventricular systo-diastolic abnormality on instrumental exams. Left ventricular volume is within normal upper limits on TTE, with good contractility and normal diastolic sex- agematched intervals. Myocardial mass, wall
stress, left ventricular contractility and stiffness and compliance are all normal and in
agreement with the kind of sports training.
A mean velocity mid-end-diastolic backflow
into the left atrium was recorded on TTE,
by the Valsalva maneuver, during HR
downfall, when the RR interval was over 2
seconds.
These 5 cases with different morphofunctional situations (competitive athete
versus patient waiting for heart transplant)
have diastolic mitral regurgitation in common40-42.
Table IIIA. Patients clinical charatteristics.
N° tot
Age
BS
Patology
Mt In
Ao In
Tr In
LV/Ao grad
BEM
Gr. A
Gr. B
20
20.87 ± 0.78
1.84 ± 0.08
No
0.8 ± 0.4
No
0.5 ± 0.06
No
No
16
49.9 ± 7.8
1.77 ± 0.1
No
0.5 ± 0.2
No
0.5 ± 0.1
No
No
BS = body surface; Mt In = mitralic regurgitation; Ao
In = aortic regurgitation; Tr In = tricuspidal regurgitation; LV/Ao grad = left ventricular/aorta gradient;
BEM = Endomyocardial biopsy.
166
Figure 2.
Diastolic mitral regurgitation: a borderline case in cardiovascular physiology
Discussion
The hemodynamic assumptions leading to
the onset of diastolic mitral regurgitation are
still unclearly defined, despite several works
reporting such occurrence46-53.
Such works are dealing with cases of midend-diastolic mitral regurgitation, in patients
either affected by slow rhythm disturbance
like III degree AV block or by severe aortic
regurgitation or by dilated cardiomyopathy.
Such backflow is due to atrioventricular pressure gradient inversion because of abnormal
increase in left enddiastolic ventricular pressure. Some authors54, monitoring heart cycle
by echocardiodoppler examination and intracavitary pressure by invasive method, have
found out that in patients with III degree AV
block atrial systoles, during ventricular diastole, are responsible for the atrioventricular
gradient inversion during the next atrial diastole54. The latter study explains diastolic mitral regurgitation found out in case 1, in our
study. In case 2, mitral diastolic regurgitation
is attributable to volumetric competition between aortic regurgitation and transmitral
flow to left ventricular filling, which, during
phases with low HR, leads to an abnormal
and sudden increase in mid-end-diastolic
pressure, and, therefore, to a ventricle/atrium
gradient inversion39,44,55. This event not associated to premature mitral closure, since the
ventricle is still distended, is the cause of such
regurgitation40,41;56-58.
Cases 3 and 4 deal with two patients affected by class III NYHA ischemic dilated cardiomyopathy, for whom we assume59 a physiopathologic mechanism alike massive aortic
regurgitation; the fast bloodflow into a left
noncompliant ventricle brings on a sudden increase in mid-end-diastolic pressure, which in
the course of bradycardia causes pressure
gradient inversion with backflow into the left
atrium.
In a communicating vessels system, liquids
motion is directly proportional to the actual
hemodynamic gradient40,41. A liquid motion
change or inversion can only be assumed as
related to a change in pressure gradient.
Ventricular diastole is made up of an active
and a passive phase, during which heart muscle, by its compliance (or elasticity/stiffness)
goes back to its resting conditions. Several
factors help in determining left ventricular
pressure/volume curve during diastole.
Relaxation velocity and diastolic suction are
the key factors in the early phase of diastole,
whereas myocardial stiffness/elasticity, pericardial status, pulmonary engorgement and
coronary engorgement help in the late phase
of diastole. We have found out a backflow
through the atrioventricular valves during the
second phase of diastole in four heart failure
patients and in one highly trained competitive athlete. During diastole blood, due to the
pressure gradient, flows from the atrium to
the ventricle with a variable speed according
to the diastolic phase, and especially depends
from “wall stiffness” and “chamber stiffness”.
Ventricular filling speed tapers with intraventricular pressure increase, therefore as atrium/ventricle gradient downfalls.
Speed decreases till bloodflow stops upon
reaching pressure equilibrium; upon that
while the inversion of flow direction can occur only if intraventricular pressure increases,
that is, a communicating vessels gradient inversion starts.
The above would not happen if the ventricle went on keeping its diastolic wall adaptability/distensibility. Indeed, we find diastolic
mitral regurgitation occurs, in the disease
states outlined, owing to sudden and transitory factors (aortic regurgitation massive volume, blood volume thrust forward by an atrial systole in excess); the literature16 explains
the above owing to an increase in mid-end-diastolic pressure, due to lack of ventricular
elastic skill to fit for that amount of blood
volume. Ventricular systo-diastolic failure in
these patients brings on the event.
Case 5 deals with a 45 years old subject, in
good cardiocirculatory conditions, with highly trained marathon-running competivity.
TTE shows normal morphofunctional values.
Despite this, during Valsalva maneuver or
carotid sinus stimulation such as to bring on
transitory bradycardia (30/m’) with II degree
AV block, we find the occurrence of diastolic
mitral regurgitation after a blocked atrial systole.
In order to explain this backflow in a
healthy heart, a long ventricular diastole and
an intervening blocked atrial systole won’t be
enough to increase mid-end-diastolic pressure and invert pressure gradient. Indeed a
heart bearing heavy loads, owing to the high
weekly training, which shows no abnormal
167
N. Alessandri, S. Mariani, F.R. Messina, G. Rondoni, E. Gerbasi, L. Battista, C. Gaudio
functional parameters on medical checkups,
surely can volumetrically fit for a sudden
change in 15-20% of the whole ventricular
volume. Ventricular adaptation of healthy
hearts, during mid-end-diastole37,38, as for volume load changes, is striking. Even in perfectly normal hearts there is a distensibility
threshold of myocardial fibers, likely corresponding to their resting length, beyond
which they cannot stretch.
In conclusion, our study has observed and
confirmed the existence of diastolic mitral regurgitation in several diseases, but also in a
normal cardiocirculatory condition. The
above is not related to a shear scientific curiosity but helps to confirm all we know
about cardiac cycle, and especially about diastolic function14,15,20,42. Moreover it allows us
to assume, given the scanty instrumental data
concerning this case, there could be, in normal conditions, a borderline threshold in distensibility which cannot be changed even by
extreme situations of fleeting volume change
variation.
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