The Framingham Offspring Study: a commentary. 1980.

Forty-three of 1,312 men aged 35 to 54 years in the Framingham Offspring Study had clinically recognized coronary heart disease at the initial examination. Twenty-six men in this group had previously had a myocardial infarction. Of 1,296 women in the same age range, only 11 had coronary disease and 3 a prior myocardial infarction. The prevalence of coronary heart disease in men was strongly associated with age, smoking, high density lipoprotein (HDL), low density lipoprotein (LDL) and total cholesterol using univariate analyses. When multivariate logistic regression analysis was used, age, smoking and HDL and LDL cholesterol retained their significant association with coronary heart disease. The total cholesterol/HDL cholesterol ratio was also strongly associated with coronary heart disease in the multivariate analysis. It is concluded that both HDL and LDL cholesterol are strongly and independently associated with the prevalence of coronary heart disease, whereas the level of very low density lipoprotein cholesterol makes no statistically significant independent contribution.

Lipid lowering: the case for identifying and treating the high-risk patient.

The rationale for the identification and aggressive treatment of lipid disorders in the patient with established vascular disease is thoroughly convincing. Elevated LDL cholesterol level is one of the few risk factors for which there is evidence of involvement in endothelial dysfunction, smooth-muscle proliferation, plaque destabilization, and thrombosis. Longitudinal studies have identified the role of elevated LDL cholesterol and low HDL cholesterol levels in the natural history of coronary artery disease. Clinical trials have successfully tested the feasibility of preventing coronary events using diet therapy or cholesterol-lowering drugs. These experiments have used a variety of end points, including myocardial infarction, cardiac death, total mortality rate, progression and regression of coronary artery stenoses, and progression of extracardiac atherosclerotic disease. The results are strikingly consistent. Economic analyses of the cost-benefit ratios also support these interventions in high-risk patients. These analyses also suggest that patients at high risk for coronary disease prior to its symptomatic presentation may be identified and treated to provide additional avenues for cost-effective primary prevention of this disease. The cardiologic community cannot ignore these results while embracing interventions such as angioplasty, coronary artery disease, antiarrhythmic therapy, and so forth. The scientific basis of cardiology demands the integration of techniques to control the atherosclerotic disease process itself, rather than merely the symptoms that it produces. Cardiology practices must reorganize to allow these proven interventions to become an integral part of comprehensive cardiologic care.

Left ventricular dysfunction in ischemic heart disease: fundamental importance of the fibrous matrix.

The contractile function of the myocardium is coordinated by a fibrous matrix of exquisite organization and complexity. In the normal heart, and apparently in physiological hypertrophy, this matrix is submicroscopic. In pathological states changes are frequent, and usually progressive. Thickening of the many elements of the fine structure is due to an increased synthesis of Type I collagen, This change, which affects the myocardium in a global manner, can be observed by light microscopy using special techniques. Perivascular fibrosis, with an increase in vascular smooth muscle, is accompanied by development of fibrous septa, with a decrease in diastolic compliance. These structural changes are believed to be due to increased activation of the renin-angiotensin-aldosterone system, and to be independent of the processes of myocyte hypertrophy. Reparative or replacement fibrosis is a separate process by means of which small and large areas of necrosis heal, with the development of coarse collagen structures, which lack a specific organizational pattern. Regarding ischemic heart disease, an increase in tissue collagenase is found in experimental myocardial "stunning" and in the very early phase of acute infarction. Absence of elements of the fibrous matrix allow for myocyte slippage, and--if the affected area is large--cardiac dilatation. If, subsequently, the necrosis becomes transmural, there is further disturbance of collagen due to both mechanical strain and continued autolysis, During healing collagen synthesis increases greatly to allow for reparative scarring in the available tissue matrix. In cases of infarction with moderate or severe initial dilatation, pathological hypertrophy of the spared myocardium is progressive, accounting for late heart failure and poor survival.(ABSTRACT TRUNCATED AT 250 WORDS)

The technique of inserting a Swan-Ganz catheter. Selecting the equipment; positioning the catheter properly.

Before hemodynamic monitoring, carefully select and test the appropriate equipment and calibrate all monitors. To insert the catheter, use strict aseptic technique and, whenever possible, fluoroscopic guidance. The internal jugular vein is generally preferred for cannulation, but cutdown of an antecubital vein may be better for patients receiving anticoagulants or thrombolytics. The balloon remains deflated until the catheter tip is in the right atrium. Characteristic pressure wave forms signal the catheter's passage through each heart chamber. In most patients, advancement from the right atrium to wedge position is completed within 20 to 30 seconds.

What role today for hemodynamic monitoring? When is this procedure indicated? How much training is required?

Hemodynamic monitoring is an important adjunct to clinical evaluation. Nevertheless, it should not be performed unless the derived data are needed to establish a diagnosis or guide treatment. Successful use of the flotation catheter requires technical skill in insertion and maintenance, knowledge of cardiopulmonary physiology, an understanding of potential complications (and their avoidance), and the ability to correctly interpret and apply results. To maintain competence, physicians should perform at least 50 procedures a year. It is unlikely that a large clinical trial of the general efficacy of hemodynamic monitoring could ever be conducted; however, more limited studies could help define the role of this procedure in certain settings.

Deciding when hemodynamic monitoring is appropriate. How will the data affect your diagnostic or therapeutic approach?

Hemodynamic data can be used to differentiate a variety of cardiopulmonary disorders, including right ventricular dysfunction, massive pulmonary embolism, and precapillary pulmonary hypertension. In patients with acute pulmonary edema, low-output states, or shock, hemodynamic measurements can help guide therapy; they also provide a precise estimate of a patient's response to vasoactive or inotropic drugs. Consider a flotation catheter for patients with complicated MIs, critically ill patients with multiorgan or major organ dysfunction, and high-risk cardiac patients undergoing surgery.

Left ventricular systolic and diastolic dysfunction in the acute phases of myocardial ischaemia and infarction, and in the later phases of recovery. Function follows morphology.

Myocardial ischaemia and infarction result in major changes in myocardial function, due to the metabolic and structural cause. The observed morphological changes may be macroscopic--as in clinical myocardial infarction, microscopic--as in severe, prolonged ischaemia, or ultramicroscopic--in regard to the collagen matrix. Recognition of the vulnerability of these structures to the metabolic and mechanical stresses associated with severe ischaemia or infarction allows an understanding of the processes of acute dilatation, late adverse remodelling and compensatory hypertrophy, which determine both systolic and diastolic dysfunction and define the principal clinical complications. Morphology--'Form'--is the primary determinant of function, while metabolic and other factors are secondary, variably dependent on the integrity of structure.

Guidelines for judicious use of electrocardiography. A summary of recommendations from the ACC/AHA Task Force Report.

Electrocardiography continues to be a cornerstone in the management of an array of cardiac and noncardiac disorders. However, the ease with which an electrocardiogram can be obtained, as well as its low cost, has led to widespread use--and possible overuse--of this technology. A joint committee of the American College of Cardiology and the American Heart Association recently published guidelines for appropriate use of electrocardiography in patients with known heart disease; in persons suspected of having, or who are at risk for, heart disease; and in persons with no apparent or suspected cardiac disease. These guidelines can help clinicians determine when, and for which patients in the intensive care unit, an electrocardiogram is warranted.

The pulmonary artery catheter.

First developed more than 20 years ago as a research tool for investigations of myocardial infarction, the pulmonary artery or Swan-Ganz catheter has gained general usage as a valuable clinical tool. Its development paralleled the rapid growth of technological advancements in clinical medicine. Rapid incorporation of technological advancements into clinical practice, however, is not without risk. Care must be taken to assure that clinicians possess the understanding of both basic concepts and requisite hardware to provide quality patient care. Equipment selection and calibration, patient selection, data interpretation, potential complications, troubleshooting, and procedure limitations must all be considered. Broader application of the Swan-Ganz catheter in surgery, anesthesiology, and critical care as well as in cardiology has provided information on hemodynamics that has had considerable impact on diagnostics as well as on therapy for patients with a wide variety of clinical conditions.

New method for monitoring pulmonary artery catheter location.

OBJECTIVE: To test the ability of a modified pulmonary artery (PA) monitoring catheter to detect distal catheter migration. DESIGN: Prospective nonrandomized trial. PATIENTS: Surgical ICU patients requiring invasive hemodynamic monitoring. INTERVENTIONS: Eight patients received PA catheters modified to include a right ventricular (RV) pressure monitoring port located 7 cm from the tip. Fifteen patients received catheters with an RV port located 10 cm from the tip. Guided by the RV port pressure waveform, catheters were initially positioned so that the RV port was located just proximal to the pulmonic valve. MEASUREMENTS AND MAIN RESULTS: Pulmonary capillary occlusion pressure (PAOP) could not be obtained in six of the eight patients receiving the 7-cm RV port catheter unless the RV port was advanced into the PA. PAOP was consistently obtained in all 15 patients receiving the 10-cm RV port catheter, with the RV port positioned in the RV. Chest radiographs confirmed a central PA catheter position. In this group, distal migration of the catheter occurred 14 times in eight patients, as detected by appearance of a PA pressure waveform at the RV port. Distal migration was corrected by withdrawal of the catheter until an RV waveform reappeared at the RV port. CONCLUSIONS: We conclude that distal catheter migration occurs frequently with PA monitoring catheters, but can be detected at the bedside with a catheter modified to include an RV port 10 cm from the tip. This new catheter may add a margin of safety to PA monitoring and lower its overall cost by eliminating the need for chest radiographs ordered solely to confirm catheter tip location.

The technique of percutaneous transluminal coronary angioplasty. Uses, abuses, training requirements, benefits, complications.

Like coronary artery bypass grafting, PTCA is used to manage multilesion and multivessel disease, new complete occlusions, and partial occlusions of saphenous vein or internal mammary artery grafts. PTCA is contraindicated for patients with a significant obstructive lesion in the left main coronary artery or with severe diffuse atherosclerosis. In determining whether this procedure provides the best treatment option, the risk of abrupt vessel closure, restenosis, MI, or incomplete revascularization must be considered. Guidelines for the performance of PTCA and physician and institutional responsibilities have been established; these guidelines must be regarded as necessary criteria for wide adoption.

Can heart failure be prevented, delayed, or reversed?

A review of the clinical course of chronic heart failure demonstrates that current outcomes remain highly unsatisfactory both in mortality and perhaps more important in morbidity. The extraordinary satisfactory functional responses seen in patients who undergo cardiac transplantation clearly identify the primary cause as the status of the heart itself, whatever the pathophysiologic adjustments of the neuroendocrine system, and interventions of the wide variety of drugs. Since donor hearts are unlikely to be available even from younger sufferers of these clinical syndromes, prevention must be the hallmark. Protection of the viability of myocytes, such as in acute myocarditis and acute infarction, is essential. Myocardial collagen undergoes continual synthesis, and production is greatly stimulated in the presence of hypertrophy caused by increased wall stress. It is possible that excess collagen is intimately involved with diastolic ventricular dysfunction, but that this may be a reversible process if the collagen-producing stimulus is removed. Thus reduction in wall stress and reversibility of ventricular hypertrophy appear to be promising directions. However, to limit the catastrophic effects of chronic heart failure, early recognition of the precursors of these syndromes, prevention of progression, and surgical intervention in valvular heart disease at an optimal point in time are essential.