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<p><b>OBJECTIVE</b>To compare the features of patients with pulmonary hypertension due to left heart disease classified according to transpulmonary gradient (TGP) or diastolic pressure difference (DPD).</p><p><b>METHODS</b>Thirty-three patients with pulmonary hypertension due to left heart disease diagnosed by right heart catheterization were enrolled. Patients were divided into two groups according to TPG: 17 patients with TPG ≤ 12 mmHg (1 mmHg = 0.133 kPa) and 16 patients with TPG > 12 mmHg; or divided into two groups according to DPD: 23 patients with DPD < 7 mmHg and 10 patients with DPD ≥ 7 mmHg. McNemar's method was used to test the agreement of the two classification methods.</p><p><b>RESULTS</b>Below are the patients features according to the classification by TPG: central venous pressure ((9.0 ± 2.5) vs. (12.7 ± 5.4) mmHg), mean right atria pressure ((9.1 ± 2.4) vs. (12.8 ± 5.2) mmHg), right heart systolic pressure ((45.5 ± 9.8) vs. (66.8 ± 15.4) mmHg), right heart mean pressure ((22.6 ± 5.2) vs. (33.1 ± 7.5) mmHg), pulmonary systolic pressure ((44.2 ± 10.3) vs. (64.8 ± 14.2) mmHg), pulmonary diastolic pressure ((24.2 ± 4.5) vs. (33.1 ± 8.3) mmHg), pulmonary mean pressure ((32.3 ± 5.7) vs. (45.8 ± 8.6) mmHg), cardiac index ((2.6 ± 1.0) vs. (1.9 ± 0.9) L · min(-1) · m(-2)), right heart EF ((31.2 ± 12.6)% vs. (22.6 ± 7.1) %) and pulmonary vascular resistance ((2.3 ± 0.8) vs. (6.3 ± 2.6) Wood) were significantly different between the two groups (all P < 0.05). According to the classification of DPD, only right heart diastolic pressure ((7.4 ± 3.7) vs. (11.5 ± 5.7) mmHg), pulmonary diastolic pressure ((25.9 ± 6.4) vs. (34.7 ± 8.0) mmHg) and pulmonary vascular resistance ((3.3 ± 2.0) vs. (6.2 ± 3.4) Wood) were significantly different between the two groups (all P < 0.05). These was a weak agreement (κ = 0.386 6, 95% CI: 0.092 2-0.681 0) between the two classification methods.</p><p><b>CONCLUSION</b>TPG classification is superior to DPD classification for pulmonary hypertension patients due to left heart disease on identifying the hemodynamic differences.</p>
Subject(s)
Humans , Blood Pressure , Cardiac Catheterization , Diastole , Heart , Heart Failure , Hemodynamics , Hypertension, Pulmonary , Vascular ResistanceABSTRACT
Objective Chronic atrial fibrillation (AF) results in dedifferentiation of atrial cardiomyocytes that plays an important role in the perpetuation of AF.In this study,we aimed to investigate the changes of titin and α-smooth muscle actin (α-SMA) after long time of AF reversal.Methods Twenty-four goats were randomized into four groups:(1) sinus rhythm (SR),(2) 3 months AF (3-mo AF),(3) 3 months SR after 3 months AF (3-mo post AF),(4) 6 months SR after 3-mo AF (6-mo post AF),with 6 in each group.By pacing on the anterior bottom of left atria appendage (LAA),we established a goat model of chronic AF.Atria effective refractory period (AERP) was measured with electrophysiological methods.Ultra-structure was studied with echocardiography,light and electron microscopy.Titin and α-SMA protein expressions were determined by Western blot.Results The animals underwent high rate pacing on LAA for a mean of 42.23±21.70 days before presenting AF.Electrophysiological analysis revealed that AERP completely resumed in 3-mo post AF goats.Echocardiography displayed that the size of left atrium resumed almost in 6-mo post AF goats (P＜ 0.01).Pathological and electron microscopic examination revealed the disorder of myofibrils,augmentation of intercellular space,myolysis,accumulation of glycogen,and numerous bigger mitochondria among atrial cardiomyocytes in 3-mo AF goats.They recovered mostly in 6-mo post AF goats.Western blot showed that the band density of titin significantly reduced in 3-mo AF goats compared to SR ones [1826±319 vs 5012±854,P＜0.01].In 3-and 6-mo post AF goats,titin increased gradually and it reversed completely in 6-mo post AF goats (3841±601 and 4523±833 respectively,P ＜ 0.01).Conversely,the band density of α-SMA was significantly higher in 3-mo AF goats (5324±948) than in SR ones (1619± 271,P＜0.01).In 3-and 6-mo post-AF goats,α-SMA decreased gradually,and it recovered mostly in 6mo post AF goats (4437± 792 and 2205±540 respectively,P＜0.01,).Conclusions These data indicate that the reversal of dedifferentiation of atrial cardiomyocyts is a very slow process,and it is definitely essential for normal cardiac function.
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Despite of great advances in drug management of heart failure in the past ten years,the condition remains a major public health issue,with high prevalence,poor clinical outcomes.Treatment of established systolic chronic heart failure includes agents that block the renin-angiotensin-aldosterone and sympathetic nervous systems to prevent adverse remodelling,to reduce symptoms and prolong survival.Diuretics,Vasodilator and Digoxin are often used to improve sign,with no influence on prognosis.Pharmacological agents aimed at new targets on clinically relevant endpoints are going under investigating.
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Objective To explore the mechanism of macro-reentry atrial tachycardia and to guide catheter ablation using electroanatomic mapping system in 3 patients.Methods Three patients(two females),aged 51?12 years,with atrial tachycardia were included.The mean history of symptom was 19?11 years.Conventional electrophysiological study was performed to determine the location of atrial tachycardia before the three dimensional geometry reconstruction.After voltage and activation maps were constructed,the mechanism of tachycardia was analyzed and the slow conduction areas(critical isthmus) were verified.Radiofrequency energy was delivered using irrigated-tip catheter.Results Though there was no evidence to suggest structural heart diseases,scar areas were found in the mapped atria in all the three cases.The mechanism of atrial tachycardia was found to be counter-clockwise macro-reentry around tricuspid valve,counter-clockwise macro-reentry around superior vena cava,and figure "8" reentry in left atria in the 3 patients respectively.The respective critical isthmus was found to be between the lateral scar and tricuspid valve,the lateral scar and superior vena cava,and two scars on the left atria roof.Ablation in the critical isthmus terminated all tachycardia.There were no atrial tachycardia recurrence during a follow-up of 9-10 months.Conclusion The substrate and electrophysiological mechanism of macro-reentry atrial tachycardia could be identified clearly,and navigation ablation could be performed effectively under the guidence of electroanatomic mapping.