Cardiac hypertrophy: Useful adaptation or pathologic process?

An extensive body of evidence supports the concept that cardiac hypertrophy and normal cardiac growth develop in response to increased hemodynamic loading and abnormal systolic and diastolic stresses at the myocardial fiber level. The pattern of hypertrophy reflects the nature of the inciting stress. Experimental studies indicate that if the stress is moderate, gradually applied, and the animal young and healthy, physiologic hypertrophy of muscle with normal contractility develops. In this circumstance, cardiac hypertrophy may be regarded as a useful adaptation to increased hemodynamic loading. When the inciting stress is severe, abruptly applied, or the animal old or debilitated, pathologic hypertrophy develops: in this circumstance, the cardiac muscle produced is abnormal and exhibits depressed contractility. Of particular clinical relevance is the intermediate situation which seems to develop in many patients with chronic left ventricular pressure-overload and perhaps also in left ventricular volume-overload. In this situation, chronic left ventricular pressure or volume overload is initially matched by adequate hypertrophy in the appropriate pattern. Eventually, in some patients, hypertrophy fails to keep pace with the hemodynamic overload so that a systolic stress imbalance occurs at the myocardial fiber level and left ventricular pump failure ensues. If this situation persists uncorrected, it is possible that the increasingly high wall stresses will convert physiologic to pathologic hypertrophy. The task of the clinician is to identify this intermediate stage and to correct the abnormal hemodynamic loading before the transition to pathologic hypertrophy becomes complete.     

Demonstration of re-entry within the canine specialized conduction system.

There is suggestive evidence that bundle branch re-entry occurs in man in response to premature right ventricular stimulation. Demonstration of the activation sequence during re-entrant excitation in the in vivo dog was accomplished by placing recording electrodes on the major portions of the specialized conduction system. A temporary right heart bypass was utilized to place two or more electrodes on both right and left bundle branches and place electrodes on the His bundle and on the left and right ventricular endocardium. Premature excitation of the right ventricle was found not to retrogradely activate the right bundle but was able to cause slow right to left myocardial activation that resulted in retrograde activation within the left bundle branch. Retrograde conduction in the left bundle caused activation of the His bundle and the proximal right bundle. Activation of the right bundle resulted in antegrade conduction of the impulse across the site of previous conduction block and re-excitation of the right ventricle, to complete the re-entrant circuit. This type of re-entry, utilizing the bundle branches, was demonstrated in 19 dogs. This re-entry circuit was found to be facilitated by shortening of the right ventricular refractory period by local epicardial warming and was abolished by interruption of conduction in the right bundle by anodal blocking current applied to the right bundle. The sites of slow conduction, site of unidirectional block, and pathways of conduction were demonstrated. The validity of the concept of re-entry occurring within the specialized conduction system is substantiated.     

Pulmonary hypertension in systemic lupus erythematosus: Report of four cases and review of the literature

Pulmonary hypertension has been reported rarely in patients with systemic lupus erythematosus (SLE). During the past 3$\text{1}\text{2}$ yr we have observed pulmonary hypertension as a major clinical manifestation of their disease in four of 43 patients with well-documented SLE followed at our institution.Pulmonary hypertension could be atrributed to underlying lung disease in three and was considered to be primary in the remaining patient. Neither hydralazine nor prednisone administration had any effect on the course of the pulmonary hypertension in these patients.The presence of pulmonary hypertension in the course of active SLE may be more common than previously recognized.     

Predictors of hospital transfer and associated risks of mortality in acute pancreatitis

BackgroundThere is limited research in prognosticators of hospital transfer in acute pancreatitis (AP). Hence, we sought to determine the predictors of hospital transfer from small/medium-sized hospitals and outcomes following transfer to large acute-care hospitals.MethodsUsing the 2010–2013 Nationwide Inpatient Sample (NIS), patients ≥18 years of age with a primary diagnosis of AP were identified. Hospital size was classified using standard NIS Definitions. Multivariable analyses were performed for predictors of “transfer-out” from small/medium-sized hospitals and mortality in large acute-care hospitals.ResultsAmong 381,818 patients admitted with AP to small/medium-sized hospitals, 13,947 (4%) were transferred out to another acute-care hospital. Multivariable analysis revealed that older patients (OR = 1.04; 95%CI 1.03–1.06), men (OR = 1.15; 95%CI 1.06–1.24), lower income quartiles (OR = 1.54; 95%CI 1.35–1.76), admission to a non-teaching hospital (OR = 3.38; 95%CI 3.00–3.80), gallstone pancreatitis (OR = 3.32; 95%CI 2.90–3.79), pancreatic surgery (OR = 3.14; 95%CI 1.76–5.58), and severe AP (OR = 3.07; 95%CI 2.78–3.38) were predictors of “transfer-out”. ERCP (OR = 0.53; 95%CI 0.43–0.66) and cholecystectomy (OR = 0.14; 95%CI 0.12–0.18) were associated with decreased odds of “transfer-out”.Among 507,619 patients admitted with AP to large hospitals, 31,058 (6.1%) were “transferred-in” from other hospitals. The mortality rate for patients “transferred-in” was higher than those directly admitted (2.54% vs. 0.91%, p < 0.001). Multivariable analysis revealed that being “transferred-in” from other hospitals was an independent predictor of mortality (OR = 1.47; 95% CI 1.22–1.77).ConclusionsPatients with AP transferred into large acute-care hospitals had a higher mortality than those directly admitted likely secondary to more severe disease. Early implementation of published clinical guidelines, triage, and prompt transfer of high-risk patients may potentially offset these negative outcomes.     

Health Care Resource Utilization Among Children With Congenital Heart Disease: A Population-Based Study

Background

Data regarding health care resource utilization (HRU) in early childhood among children with congenital heart disease (CHD) are scarce. Therefore, we sought to describe the extent of HRU incurred among children with CHD in the first 5 years of life.

Evidence for a flow-independent contribution to the phenomenon of thallium redistribution

Although thallium-201 is known to redistribute slowly into regions of ischemic myocardium after restoration of blood flow, it is not clear to what extent normalization of flow is an essential requirement for the redistribution process. In a search for a flow-independent component of thallium redistribution, 12 dogs with stenosis of the circumflex coronary artery underwent atrial pacing for either 20 minutes (group I, 6 dogs) or 2 hours (group II, 6 dogs). Radioactive thallium and radioactive microspheres, 7 to 10 μ, were injected after 10 minutes of atrial pacing in both groups. Pacing resulted in a 40 percent reduction in subendocardial blood flow to the circumflex-perfused myocardium in both groups I and II. This relative reduction in flow was maintained at a stable level over the 2 hour pacing period in group II. Thallium activity in the relatively ischemic zone was significantly greater in dogs with 2 hours of pacing (group II) than in those with 10 minutes of pacing (group I). Redistribution of thallium occurred despite the continued presence of reduced flow in circumflex-perfused endocardial tissue. These data suggest that a significant component of thallium redistribution may be flow-independent.     

Alteration of pulmonary function in intravenous drug abusers: Prevalence,severity, and characterization of gas exchange abnormalities

We examined the influence of chronic intravenous drug abuse on respiratory function in 512 consecutive drug addicts by obtaining respiratory histories, pulmonary function tests and chest roentgenograms. Two hundred and fourteen (42 per cent) had carbon monoxide-diffusing capacities (D_lco) of < 75 per cent predicted (mean 65.7 per cent), and in 38 per cent reduced D_lco was the sole pulmonary function test abnormality. Obstructive lung disease attributed to asthma or chronic bronchitis was observed in 6 per cent and a restrictive defect due to interstitial lung disease was observed in 7 per cent. Exercise limitation due to dyspnea among those patients with altered pulmonary function was uncommon except in those with obstructive or restrictive lung disease. Roentgenographic evidence of pulmonary hypertension was not observed in any of the patients. Gas exchange measured at rest and during exercise in 11 patients with a low D_lco and in three patients with restrictive lung disease and a low D_lco revealed an increased alveolar-arterial oxygen difference but normal minute ventilation, dead space-to-tidal volume ratio and absence of abnormal right-to-left shunts. We conclude that alterations in pulmonary function in drug addicts due to foreign particle emboli are very common but that significant respiratory symptoms are unusual and that abnormalities in gas exchange during exercise are mild.