Left Ventricular End-Diastolic Pressure-Volume Relationships in Hypertrophic Cardiomyopathy

CHEST Journal ◽  
1983 ◽  
Vol 84 (1) ◽  
pp. 54-57 ◽  
Author(s):  
Michael Tendera ◽  
Lech Polonski ◽  
Ewa Kozielska
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Diastolic Pressure ◽  
Left Ventricular

scholarly journals Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP, in hypertrophic cardiomyopathy

2006 ◽  
Vol 290 (3) ◽  
pp. H1064-H1070 ◽  
Author(s):  
Shinsuke Kido ◽  
Naoyuki Hasebe ◽  
Yoshinao Ishii ◽  
Kenjiro Kikuchi
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Myocardial Ischemia ◽  
Diastolic Dysfunction ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Catheter Tip ◽  
Lv Systolic Function ◽  
Lv Diastolic Dysfunction

The aim of this study was to investigate what factor determines tachycardia-induced secretion of atrial and brain natriuretic peptides (ANP and BNP, respectively) in patients with hypertrophic cardiomyopathy (HCM). HCM patients with normal left ventricular (LV) systolic function and intact coronary artery ( n = 22) underwent rapid atrial pacing test. The cardiac secretion of ANP and BNP and the lactate extraction ratio (LER) were evaluated by using blood samples from the coronary sinus and aorta. LV end-diastolic pressure (LVEDP) and the time constant of LV relaxation of tau were measured by a catheter-tip transducer. These parameters were compared with normal controls ( n = 8). HCM patients were divided into obstructive (HOCM) and nonobstructive (HNCM) groups. The cardiac secretion of ANP was significantly increased by rapid pacing in HOCM from 384 ± 101 to 1,268 ± 334 pg/ml ( P < 0.05); however, it was not significant in control and HNCM groups. In contrast, the cardiac secretion of BNP was fairly constant and rather significantly decreased in HCM ( P < 0.01). The cardiac ANP secretion was significantly correlated with changes in LER ( r = −0.57, P < 0.01) and tau ( r = 0.73, P < 0.001) in HCM patients. Tachycardia potentiates the cardiac secretion of ANP, not BNP, in patients with HCM, particularly when it induces myocardial ischemia and LV diastolic dysfunction.

scholarly journals Coronary Arteriographic Profile in Hypertrophic Cardiomyopathy (HCM)

2004 ◽  
Vol 3 (3) ◽  
pp. 24
Author(s):  
Iqbal Hasan ◽  
KMHSS Haque ◽  
Shaffiuddin Ahmed ◽  
MA Siddique ◽  
SK Banerjee ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Hypertrophic Cardiomyopathy ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Cross Sectional Study ◽  
Left Ventricular ◽  
Military Hospital ◽  
Cross Sectional ◽  
Ventricular Systolic Pressure ◽  
Coronary Patients

This cross-sectional study was carried out in department of cardiology, Combined Military Hospital, Dhaka, Bangladesh and department of cardiology, Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh during the period of April 2000 to November 2001. The study was designed to see the coronary arteriographic (CAG) pattern in patients with Hypertrophic Cardiomyopathy and to compare the CAG findings between HCM patients and normal coronary patients, HCM was diagnosed by using diagnostic criteria defined by Western Working Group. The patients with hypertention, congenitalheart disease, valvular heart disease, coronary artery disease were excluded from the study. Among total 60 subjects, 30 had HCM and 30 age and sex matched control. The mean age of cases was 45.00±15.38 years and control subjects was 44.35±15.14 years. HCM cases had significantly higher left ventricular systolic pressure, higher left ventricular end diastolic pressure and more ejection fraction than control. Origin of coronary artery both in control and HCM cases were normal.

scholarly journals Biphasic changes in left ventricular end-diastolic pressure during dynamic exercise in patients with nonobstructive hypertrophic cardiomyopathy

2001 ◽  
Vol 38 (2) ◽  
pp. 335-343 ◽  
Author(s):  
Yasushi Takeichi ◽  
Mitsuhiro Yokota ◽  
Mitsunori Iwase ◽  
Hideo Izawa ◽  
Takao Nishizawa ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise

Prognostic significance of left ventricular end diastolic pressure using E/E' in patients with hypertrophic cardiomyopathy

2019 ◽  
Vol 36 (12) ◽  
pp. 2167-2175
Author(s):  
Hala Mahfouz Badran ◽  
Ghada Soltan ◽  
Reda Almeleigi ◽  
Naglaa Faheem ◽  
Magdi H. Yacoub
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Diastolic Pressure ◽  
Prognostic Significance ◽  
Left Ventricular

Acute Changes in Left Ventricular End Diastolic Pressure following the Transcatheter Closure of an Atrial Septal Defect in Adults

2016 ◽  
Vol 19 (3) ◽  
pp. 145 ◽  
Author(s):  
Young Hwa Kong ◽  
Jinyoung Song ◽  
Kyung Hee Kim ◽  
June Huh ◽  
I-Seok Kang
Keyword(s):  
Elderly Patients ◽  
Atrial Septal Defect ◽  
Septal Defect ◽  
Transcatheter Closure ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Device Closure ◽  
Acute Changes ◽  
Asd Closure

<strong>Background:</strong> Acute changes in left ventricular diastolic function shortly after ASD closure in elderly patients have not been well known. We aimed to investigate acute changes in left ventricular end diastolic pressure (LVEDP) in elderly patients following transcatheter closure of atrial septal defect (ASD). <br /><strong>Methods:</strong> All 19 adults with ASDs who underwent transcatheter closure between June 2013 and December 2014 were enrolled. LVEDP was measured prior to device closure and compared with that immediately following device closure and 15 minutes after device closure. <br /><strong>Results:</strong> The median age of the patients was 48 years old. The baseline E/e’ and LVEDP values were 8.3 ± 2.8 and 13 ± 3 mmHg. The LVEDP value immediately following closure was 19 ± 4 mmHg, and 15 minutes after closure was 16 ± 4 mmHg. The median increase in the LVEDP value immediately following closure was 6 mmHg, which significantly differed from that prior to closure. The LVEDP 15 minutes after closure decreased but remained significantly higher than the value observed immediately after closure. No significant changes were observed with regard to E/e’ at either 1 day or 3 months following closure. The LVEDP value <br />15 minutes after device closure was significantly correlated with those observed before closure and immediately following closure; however, no significant correlations were observed with regard to patient age, Qp/Qs, E/e’ before closure, or E/e’ 3 months after device closure.<br /><strong>Conclusion:</strong> LVEDP in adults with ASDs significantly increases following device closure. LVEDP before closure predicts LVEDP following device closure.

RELATIVE CONTRIBUTIONS OF FIBROSIS AND CONNEXIN CHANGES TOTHE ATRIAL FIBRILLATION SUBSTRATE DURING THE DEVELOPMENT AND REVERSAL OF CONGESTIVEHEART FAILURE

2008 ◽  
Vol 31 (4) ◽  
pp. 5
Author(s):  
Brett Burstein ◽  
Kunihiro Nishida ◽  
Philippe Comtois ◽  
Louis Villenuve ◽  
Yung-Hsin Yeh ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Potential Model ◽  
Diastolic Pressure ◽  
Recovery Period ◽  
Left Ventricular ◽  
Muscle Bundle ◽  
Protein Ratio ◽  
Conduction Disturbances ◽  
Conduction Abnormalities ◽  
Mrna And Protein Expression

Background: Connexin alterations occur in various atrial fibrillation (AF) paradigms, but their functional significance remains unclear. No data are available regarding the effects of CHF on atrial connexin expression and phosphorylation. We therefore analyzed connexin changes and their contribution to the AF substrate during the development and reversal ofCHF. Methods and Results: Dogs were allocated to three groups: CHF induced by 2-week ventricular tachypacing (CHF, n=15); CHF dogs allowed to recover for 4 weeks after 2-week tachypacing (REC, n=15) and non-paced shams (CTL, n=11). Left ventricular end-diastolic pressure increased with CHF (14.5±1.0*** vs.3.7±0.7, ***P < 0.001 vs. CTL) and normalized upon CHF recovery (5.1±1.0^†††, ^††† P < 0.001 vs. CHF). Real-time PCR and Western-blot analyses revealed connexin43 (Cx43) and connexin40 (Cx40) mRNA and protein expression to be unchanged by CHF and REC. However, CHF caused Cx43 dephosphorylation(by ~73%***) and increased Cx40/Cx43 protein ratio (by ~35%***), with both alterations completely reversing in REC. Immunofluorescent confocal microscopy confirmed connexin protein trends, with a reduction in phosphorylated Cx43 (by ~68%*** in CHF) that returned to control in REC. CHF caused conduction abnormalities (phasedelay-range and heterogeneity index, both P < 0.01) and burst pacing-induced AF prolongation (CTL 22±7s, CHF 1100±171s***, REC 884±220s***) which persisted in the recovery period, along with residual fibrosis (CTL 3.6±0.7%, CHF 14.7±1.5%***, REC13.3±2.3%***). Fibrosis physically interrupted muscle bundle continuity and anionically-based action potential model of canine atrium showed that fibrosiswas able to account for the observed conduction abnormalities. Conclusions: CHF causes connexin-dephosphorylation and Cx40/Cx43ratio increases. With CHF reversal, atrial connexin alterations recover completely, but tissue fibrosis, conduction abnormalities and a substrate forAF remain with fibrosis accounting for conduction abnormalities. Thus, althougha trial connexin changes occur with CHF, they are not essential for conduction disturbances and AF promotion, which appear rather to be related primarily tofibrotic interruption of muscle-bundle continuity.

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