Regression of Left Ventricular Dilation After Percutaneous Closure of a Large Intralobar Pulmonary Sequestration

2009 ◽  
Vol 20 (1) ◽  
pp. 89-90 ◽  
Author(s):  
Alejandro Alvarez ◽  
Francesco Borgia ◽  
Paolo Guccione
Keyword(s):  
Pulmonary Sequestration ◽  
Left Ventricular ◽  
Percutaneous Closure ◽  
Ventricular Dilation ◽  
Intralobar Sequestration ◽  
Left Ventricular Dilation ◽  
Intralobar Pulmonary Sequestration ◽  
Aberrant Artery ◽  
The Right ◽  
Left Ventricular Enlargement

AbstractWe describe an infant of 8 months who presented with left ventricular dilation due to an extensive intralobar sequestration of the right lung. The pulmonary sequestration was associated with a patent arterial duct and a right aortic arch. Percutaneous closure of the anomalous aberrant artery feeding the sequestrated lung resulted in prompt regression of the left ventricular enlargement.

scholarly journals Exaggerated Left Ventricular Dilation and Reduced Collagen Deposition After Myocardial Infarction in Mice Lacking Osteopontin

2001 ◽  
Vol 88 (10) ◽  
pp. 1080-1087 ◽  
Author(s):  
Nathan A. Trueblood ◽  
Zhonglin Xie ◽  
Catherine Communal ◽  
Flora Sam ◽  
Soeun Ngoy ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular ◽  
Collagen Deposition ◽  
Ventricular Dilation ◽  
Left Ventricular Dilation

Post-stress end-systolic left ventricular dilation: a marker of endocardial post-ischemic stunning

2001 ◽  
Vol 22 (6) ◽  
pp. 685-693 ◽  
Author(s):  
A. BESTETTI ◽  
C. DI LEO ◽  
A. ALESSI ◽  
A. TRIULZI ◽  
L. TAGLIABUE ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Ventricular Dilation ◽  
Left Ventricular Dilation ◽  
Post Stress

scholarly journals Collateral channels that develop after an acute myocardial infarction prevent subsequent left ventricular dilation

1996 ◽  
Vol 27 (5) ◽  
pp. 1133-1139 ◽  
Author(s):  
Kazuhisa Kodama ◽  
Hideo Kusuoka ◽  
Akihiko Sakai ◽  
Takayoshi Adachi ◽  
Shinji Hasegawa ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Left Ventricular ◽  
Ventricular Dilation ◽  
Left Ventricular Dilation

MDCT Demonstration of Intralobar Pulmonary Sequestration of the Right Upper Lobe in an Adult

2005 ◽  
Vol 185 (6) ◽  
pp. 1663-1664 ◽  
Author(s):  
Gilbert R. Ferretti ◽  
François Blanc Jouvan ◽  
Max Coulomb
Keyword(s):  
Pulmonary Sequestration ◽  
Intralobar Pulmonary Sequestration ◽  
The Right

Co-morbidity (HFrEF and HFpEF): hypertension

ESC CardioMed ◽  
2018 ◽  
pp. 1808-1812
Author(s):  
Francesco Paneni ◽  
Massimo Volpe
Keyword(s):  
Blood Pressure ◽  
Ejection Fraction ◽  
Left Ventricular ◽  
Ventricular Dilation ◽  
Hypertensive Patients ◽  
Reduced Ejection Fraction ◽  
Concentric Hypertrophy ◽  
Drug Classes ◽  
Left Ventricular Dilation ◽  
Eccentric Hypertrophy

Hypertensive heart disease is a major cause of heart failure (HF) and mortality. Hypertension precedes HF occurrence in 75% of cases, and carries a sixfold increase in HF risk as compared to non-hypertensive individuals. Most importantly, a minority of patients survive 5 years after the onset of hypertensive HF. In hypertensive patients, the heart may present different patterns of adaptive remodelling: concentric remodelling, concentric hypertrophy, and eccentric hypertrophy. Although most hypertensive patients are at high risk of developing concentric hypertrophy, a growing proportion of subjects display a concentric-to-eccentric progression eventually leading to left ventricular dilation and systolic dysfunction. Several factors including myocardial ischaemia, ethnicity, genetic background, history of diabetes, and blood pressure pattern may significantly influence the pathway from hypertension to left ventricular dilation. Patients with a concentric hypertrophy usually develop HF with preserved ejection fraction (HFpEF), whereas those with an eccentric (dilated) phenotype develop HF with reduced ejection fraction (HFrEF). Lowering blood pressure has a striking effect in reducing the risk of HF. Although available antihypertensive drugs are all successful in lowering blood pressure, angiotensin-converting enzyme inhibitors, angiotensin receptor blocker (ARBs), and diuretics are more effective than other drug classes in preventing HF. The combination of the neprilysin inhibitor sacubitril with the ARB valsartan (LCZ696) has recently been shown to be highly effective in reducing HF-related outcomes in hypertensive subjects. An individualized treatment scheme taking into account blood pressure levels, type of HF (HFpEF or HFrEF), and relevant co-morbidities (i.e. renal disease, diabetes) is currently the best approach to improve morbidity and mortality in hypertensive patients with HF.

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