Medical Consequences of Over-the-Counter (OTC) Substance Abuse
John Brick in Handbook of the Medical Consequences of Alcohol and Drug Abuse, 2012
Twelve sudden deaths in Texas were associated with chronic intravenous use of propylhexedrine. The cause was thought to be cardiac arrhythmias in combination with pulmonary hypertension and right ventricular hypertrophy. Most of the cases involved young, black males, and occasionally females (Anderson et al., 1979; White and DiMaio, 1977). Chronic injection of propylhexedrine was associated with left ventricular failure in four patients, three of whom also had right ventricular dilation, and two of whom had pulmonary hypertension. Their ages were 26 to 36 years (Croft, Firth, and Hillis, 1982).
The heart, lungs and pleura
Kevin G Burnand, John Black, Steven A Corbett, William EG Thomas, Norman L Browse in Browse’s Introduction to the Symptoms & Signs of Surgical Disease, 2014
Pulmonary regurgitation is usually acquired and may be the result of pulmonary hypertension (e.g. cor pulmonale), infective endocarditis, rheumatic fever, carcinoid syndrome or trauma (usually iatrogenic following surgery for pulmonary stenosis or tetralogy of Fallot). The symptoms that predominate are those of the underlying cause. Right ventricular hypertrophy produces a right ventricular heave on examination. The subsequent development of right heart failure produces the signs described above.
Unusual Inherited Pulmonary Diseases Which Provide Clues to Pulmonary Physiology and Function
Stephen D. Litwin in Genetic Determinants of Pulmonary Disease, 2020
Chest x ray characteristically shows an increase in size in the pulmonary artery and its main branches with rapid peripheral tapering. There is increase in the heart size with encroachment on the retrosternal clear space in the lateral projection due to right ventricular hypertrophy. The electrocardiogram invariably shows evidence of right ventricular hypertrophy.
Current and emerging imaging techniques in the diagnosis and assessment of pulmonary hypertension
Published in Expert Review of Respiratory Medicine, 2018
Christopher S. Johns, Jim M. Wild, Smitha Rajaram, Andy J. Swift, David G. Kiely
PH causes remodeling and eventual failure of the right ventricle. While right ventricular dilatation and features reflecting it’s failure are visible on CTPA, these are not features of early disease. CTPA evidence of right ventricular compromise includes dilatation of the right heart chambers, right ventricular hypertrophy (defined as wall thickness of more than 4 mm) and displacement of the IVS toward the left ventricle [40]. Changes of right ventricular hypertrophy are usually best appreciated in the right ventricular outflow tract, likely reflecting the reduced quantity of trabeculation. Reflux of contrast into the inferior vena cava and hepatic veins on contrast enhanced CT has been considered to be a marker of the severity of tricuspid regurgitation, commonly seen in PH [41], often in PH-LHD, although in the authors experience, it correlates poorly with the severity of PH. In severe pre-capillary PH, such as PAH, CTEPH and PH associated with respiratory disease (where there is severe PH) the left ventricle is under filled and compressed by the dilated RV, causing a small volume left atrium and ventricle. There may also be features of cardiac decompensation visible on CT, such as pleural and pericardial effusions, and an increase in inferior vena cava size, all of which are associated with a poor prognosis [31].
The molecular rationale for therapeutic targeting of glutamine metabolism in pulmonary hypertension
Published in Expert Opinion on Therapeutic Targets, 2019
Thomas Bertero, Dror Perk, Stephen Y. Chan
Right-sided heart failure is the primary cause of death in PAH [17,158,159], and maladaptive right ventricular hypertrophy (RVH) occurs as a consequence of increased pulmonary arterial pressure and possibly other poorly described inherent or acquired triggers. PH prognosis is directly related to the performance of the right heart [159]. Recently, it has been proposed that right ventricular hypertrophy could also be a trigger of vascular alterations in PH itself [160,161]. Specifically, increasing evidence supports the notion that right heart dysfunction may reciprocally trigger vascular manifestations of PH [17,160,161], potentially via promoting vascular stiffening and adversely affecting PA compliance. Consequently, it appears crucial to decipher the long-term evolution of cardiopulmonary interactions in PH, particularly in regard to metabolic cooperation or competition.
Elevated lipoprotein A in acute on chronic CTEPH with cardiogenic shock: a case report
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Kyaw Kyaw, Shakya Sabnam, Melanie Cheing, Fidencio Davalos, Michael Gramuglia
The admission laboratory was significant for D-dimer 2,518 ng/ml (normal 0–243 ng/ml), troponin 0.031 (normal ≤0.010 ng/ml), BUN 21 mg/dl (normal 7–18 mg/dl), Creatinine 1.3 mg/dl (normal 0.7–1.2 mg/dl), ESR 10 (normal 0–22 mm/h), CRP 1 (normal <4 mg/l) and ferritin 113 (normal 15–150 ng/ml). Chest X ray was unremarkable. The EKG reported T wave inversion in V2 to V5. CT angiogram chest showed bilateral subsegmental pulmonary embolism and mild right-heart strain (Figure 1). The echocardiogram revealed no obvious valvular abnormalities, normal left-ventricle systolic function, mild right-ventricular hypertrophy, pulmonary arterial pressure 50–55 mmHg, severe right ventricular dilatation and dysfunction (Figure 2). The hypercoagulability work-up was remarkable for elevated lipoprotein A 461.7 nmol/L (normal <75 nmol/L) and elevated homocysteine level 28.7 umol/L (normal <15 umol/L).
Related Knowledge Centers
- Ventricle
- Pulmonary Artery
- Tricuspid Valve
- Heart Failure
- Pulmonary Hypertension
- Cardiac Output
- Angina
- Syncope
- Edema
- Ortner'S Syndrome