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Biomedical subjects

Julien I E Hoffman

Publications and source records attributed to Julien I E Hoffman.

8 recordsLinked to original sources
PubMed2006

Physiological basis of clinically used coronary hemodynamic indices.

In deriving clinically used hemodynamic indices such as fractional flow reserve and coronary flow velocity reserve, simplified models of the coronary circulation are used. In particular, myocardial resistance is assumed to be independent of factors such as heart contraction and driving pressure. These simplifying assumptions are not always justified. In this review we focus on distensibility of resistance vessels, the shape of coronary pressure-flow lines, and the influence of collateral flow on these lines. We show that (1) the coronary system is intrinsically nonlinear because resistance vessels at maximal vasodilation change diameter with pressure and cardiac function; (2) the assumption of collateral flow is not needed to explain the difference between pressure-derived and flow-derived fractional flow reserve; and (3) collateral flow plays a role only at low distal pressures. We conclude that traditional hemodynamic indices are valuable for clinical decision making but that clinical studies of coronary physiology will benefit greatly from combined measurements of coronary flow or velocity and pressure.

Animals↗
PubMed2006

Myocardial protection in the failing heart: I. Effect of cardioplegia and the beating state under simulated left ventricular restoration.

OBJECTIVE: Heart failure was induced by cardiac pacing to evaluate myocardial flow distribution of the open ventricle during delivery of either cardioplegia or in the beating state during simulated left ventricular restoration. METHODS: Studies included 5 (pacing-induced) failing pig hearts and 6 control hearts. Pacing-induced cardiac failure reduced fractional shortening by approximately 22%, increased left ventricular end-diastolic diameter by 34%, caused pulmonary hypertension (mean blood pressure increased from 12 to 35 mm Hg), and led to significant ascites. Global and regional coronary blood flow were measured with microspheres during cardiopulmonary bypass at 80 mm Hg perfusion pressure in either vented (collapsed) or open (exposure by traction for left ventricular restoration) left ventricles during continuous perfusion under either beating-heart or cardioplegic conditions. RESULTS: In control hearts, venting and exposure ventriculotomy did not affect flow. In failing hearts decompressed by venting, coronary flow was lower during the beating and cardioplegic delivery than during control conditions at the same perfusion pressure of 80 mm Hg. Mean cardioplegic flow during ventricular decompression by venting exceeded beating flow by 97%. Conversely, traction to increase the ventricular radius during exposure ventriculotomy reduced endocardial cardioplegic coronary blood flow by 64% (from 0.97 to 0.59 mL/[min x g]), whereas the beating state raised endocardial flow by 95% (from 0.40 to 0.78 mL/[min x g]). Changing ventricular shape changed coronary vascular resistance in failing hearts during beating or cardioplegic delivery. CONCLUSIONS: Coronary blood flow alterations occurred only in failing hearts when geometry was changed from closed to open state. The beating method provided more endocardial flow than cardioplegic delivery during ventricular exposure for restoration. Vascular remodeling raised coronary vascular resistance in failing hearts, thereby requiring higher pressure for similar blood flows.

Animals↗
PubMed2006

Myocardial protection in the failing heart: II. Effect of pulsatile cardioplegic perfusion under simulated left ventricular restoration.

OBJECTIVE: The open ventricle was studied in pacing-induced experimental heart failure to determine the extent of coronary perfusion and distribution during either continuous or pulsatile cardioplegic perfusion compared with whole blood in the beating heart. METHODS: In 5 animals that underwent pacing-induced heart failure and in 6 control swine, regional coronary blood flows were measured on bypass in the open left ventricle (simulating exposure for left ventricle restoration) during (1) beating, (2) nonpulsatile cardioplegia, and (3) pulsatile cardioplegia modalities. Mean perfusion pressure was maintained at 80 mm Hg. RESULTS: Flow magnitude and distribution differed in control and failing hearts in the open left ventricle. In control hearts, transmural and endocardial cardioplegic flow of nonpulsatile and pulsatile flow (which were similar to each other) exceeded beating flow by 63% and 70%, respectively, in the open left ventricle condition. Transmural and subendocardial vascular resistance increased in failing hearts during cardioplegic delivery, resulting in lower subendocardial flow under nonpulsatile conditions for the same perfusion pressure. In failing hearts, subendocardial perfusion conditions did not change in the beating state (0.89 vs 0.78 mL/min/g in control and failing open beating states, respectively), but nonpulsatile cardioplegic flow was significantly reduced by 154%, and became lower than beating flow by 32.2% (0.78 vs 0.59 mL/min/g). Conversely, pulsatile cardioplegic delivery improved endocardial flow in the open failing hearts, as cardioplegic perfusion with pulsatility exceeded beating flow by 41%. In heart failure, pulsatility from either the beating heart, which causes extrinsic compression of coronary vessels, or intrinsic vessel distension during pulsatile cardioplegic perfusion preserved endocardial perfusion better than nonpulsatile cardioplegia at the same perfusion pressure. CONCLUSION: In the failing open ventricle (simulated geometry during ventricular restoration), subendocardial blood flow was maintained in the beating state, but decreased significantly from control values during nonpulsatile cardioplegic perfusion. Conversely, pulsatile cardioplegic delivery improved subendocardial perfusion of the open failing ventricle. These findings of improved subendocardial perfusion during pulsatile delivery (either during beating or cardioplegic perfusion) compared with nonpulsatile cardioplegic delivery may have important implications for myocardial protection in failing hearts.

Animals↗
PubMed2004

Prevalence of congenital heart disease.

BACKGROUND: Today most patients with congenital heart disease survive childhood to be cared for by adult cardiologists. The number of physicians that should be trained to manage these lesions is unknown because we do not know the number of patients. METHODS: To answer this question, the expected numbers of infants with each major type of congenital heart defect born in each 5-year period since 1940 were estimated from birth rates and incidence. The numbers expected to survive with or without treatment were estimated from data on natural history and the results of treatment. Finally, lesions were categorized as simple, moderate, or complex, based on the amount of expertise in management needed for optimal patient care. RESULTS: From 1940 to 2002, about 1 million patients with simple lesions, and half that number each with moderate and complex lesions, were born in the United States. If all were treated, there would be 750,000 survivors with simple lesions, 400,000 with moderate lesions, and 180,000 with complex lesions; in addition, there would be 3,000,000 subjects alive with bicuspid aortic valves. Without treatment, the survival in each group would be 400,000, 220,000, and 30,000, respectively. The actual numbers surviving will be between these 2 sets of estimates. CONCLUSIONS: Survival of patients with congenital heart disease, treated or untreated, is expected to produce large numbers of adults with congenital disease, and it is likely that many more adult cardiologists will need to be trained to manage moderate and complex congenital lesions.

Adult↗
PubMed2002

Advice on statistical analysis for Circulation Research.

Since the late 1970s when many journals published articles warning about the misuse of statistical methods in the analysis of data, researchers have become more careful about statistical analysis, but errors including low statistical power and inadequate analysis of repeated-measurement studies are still prevalent. In this review, several statistical methods are introduced that are not always familiar to basic and clinical cardiologists but may be useful for revealing the correct answer from the data. The aim of this review is not only to draw the attention of investigators to these tests but also to stress the conditions in which they are applicable. These methods are now generally available in statistical program packages. Researchers need not know how to calculate the statistics from the data but are required to select the correct method from the menu and interpret the statistical results accurately. With the choice of appropriate statistical programs, the issue is no longer how to do the test but when to do it.

Analysis of Variance↗
PubMed2002

The incidence of congenital heart disease.

This study was designed to determine the reasons for the variability of the incidence of congenital heart disease (CHD), estimate its true value and provide data about the incidence of specific major forms of CHD. The incidence of CHD in different studies varies from about 4/1,000 to 50/1,000 live births. The relative frequency of different major forms of CHD also differs greatly from study to study. In addition, another 20/1,000 live births have bicuspid aortic valves, isolated anomalous lobar pulmonary veins or a silent patent ductus arteriosus. The incidences reported in 62 studies published after 1955 were examined. Attention was paid to the ways in which the studies were conducted, with special reference to the increased use of echocardiography in the neonatal nursery. The total incidence of CHD was related to the relative frequency of ventricular septal defects (VSDs), the most common type of CHD. The incidences of individual major forms of CHD were determined from 44 studies. The incidence of CHD depends primarily on the number of small VSDs included in the series, and this number in turn depends upon how early the diagnosis is made. If major forms of CHD are stratified into trivial, moderate and severe categories, the variation in incidence depends mainly on the number of trivial lesions included. The incidence of moderate and severe forms of CHD is about 6/1,000 live births (19/1,000 live births if the potentially serious bicuspid aortic valve is included), and of all forms increases to 75/1,000 live births if tiny muscular VSDs present at birth and other trivial lesions are included. Given the causes of variation, there is no evidence for differences in incidence in different countries or times.

Ductus Arteriosus, Patent↗
PubMed2002

Abraham Morris Rudolph: an appreciation.

Dr Abraham Rudolph is one of the most distinguished pediatric cardiologists in the world. He entered pediatric cardiology (almost by accident) when the subject was still in its infancy and was present at--and indeed contributed to--most of its advances. He is best known for his studies on the pathophysiology of congenital heart diseases and for imaginative studies of fetal cardiovascular development and the transition to postnatal life.

Animals↗