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How to cite: Turina M. (1993). In response to: Grunkemeier GL, Starr A. Alternatives to randomization in surgical studies. The Journal of heart valve disease, 2(1), 123.

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How to cite: Huysmans H. (1993). In response to: Grunkemeier GL, Starr A. Alternatives to randomization in surgical studies. The Journal of heart valve disease, 2(1), 122–123.

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How to cite: Blackstone E. H. (1993). In response to: Grunkemeier GL, Starr A. Alternatives to randomization in surgical studies. The Journal of heart valve disease, 2(1), 119–122.

Aortic stenosis is a progressive disease. The mechanisms and patterns of progression have been studied over the years using clinical assessment, cardiac catheterization, and more recently, Doppler echocardiography. Doppler is the ideal tool with which to study the progression of aortic stenosis since it provides accurate hemodynamic data non-invasively and, hence, can be repeated serially over long follow up periods. Recent Doppler echocardiographic studies have shown that the progression of aortic stenosis occurs with a wide range of individual variations, and that its rate and pattern cannot be predicted at the time of initial evaluation. However, it does follow a linear pattern, and individual trends can therefore be determined in a given patient. Symptoms lack specificity and, at a given point in time, do not predict progression. However, new and/or worsening symptoms are a mark of significant hemodynamic progression. The relationship between the cause of aortic stenosis and its progression remains imperfectly documented, and further longitudinal studies should focus on this question.

How to cite: Roger, V. L., & Tajik, A. J. (1993). Progression of aortic stenosis in adults: new insights provided by Doppler echocardiography. The Journal of heart valve disease, 2(1), 114–118.

To assess left atrial volume and function in aortic stenosis, 20 patients with this condition and 10 normal controls were studied. Atrial volumes were measured by echocardiography at mitral valve opening (maximal), onset of atrial systole (P wave of the electrocardiogram) and mitral valve closure (minimal), using biplane techniques. The maximal volume was greater in those patients with aortic stenosis as compared to the controls (74.8 +/- 26.4 cm3 vs. 46.4 +/- 11.9 cm3, p < 0.005), and was directly related to left ventricular mass (r = 0.77). The passive emptying volume (maximal minus onset of atrial systole) was similar in the two groups (21 +/- 8 cm3 vs. 18.7 +/- 5.9 cm3, p = NS), while active emptying volume (onset of atrial systole minus minimal) was higher in aortic stenosis (16.8 +/- 5.2 cm3 vs. 10.2 +/- 2.5 cm3, p < 0.001). The total emptying volume (sum of passive and active) was slightly higher amongst those with aortic stenosis (37.4 +/- 10.2 cm3 vs. 28.9 +/- 7.5 cm3, p < 0.05). The passive emptying fraction (passive emptying volume/maximal) was lower in the aortic stenosis group (0.28 +/- 0.08 vs. 0.40 +/- 0.05, p < 0.001), while the active emptying fraction (active emptying volume/volume at onset of atrial systole) was similar between the two groups (0.33 +/- 0.09 vs. 0.37 +/- 0.05, p = NS). Increased left atrial size in aortic stenosis is directly related to left ventricular mass and restores left atrial total emptying volume, despite the depressed passive emptying fraction. Left atrial dilatation thus represents an important compensatory mechanism, contributing to the maintenance of left ventricular stroke volume and cardiac output in severe aortic stenosis.

How to cite: Triposkiadis, F., Pitsavos, C., Boudoulas, H., Trikas, A., Kallikazaros, I., Stefanadis, C., & Toutouzas, P. (1993). Left atrial volume and function in valvular aortic stenosis. The Journal of heart valve disease, 2(1), 104–113.

Turbulent blood flow can occur downstream from a stenosis. The purpose of this study was to quantitate turbulence intensity and its frequency characteristics in the ascending aorta in adult patients with and without valvular stenosis, and to use extrasystoles to analyze the effects of changes in left ventricular function on turbulence. Turbulence intensity was determined from the digitized, high frequency oscillations seen in high fidelity pressure recordings of 25 patients with valvular aortic stenosis. The intensity of turbulence was quantitated as the root-mean-square (mmHg) of pressure fluctuations and as the total spectral power (mmHg2/beat) of the frequency spectrum between 25 Hz and 400 Hz. Frequency characteristics were summarized by the mean and median frequency of spectral power and partitioning the spectrum into 25 Hz segments. Ten adult patients without aortic valve or outflow tract abnormalities served as controls. Adult patients with aortic stenosis had significantly more turbulence in the ascending aorta than controls (total spectral power 1577 +/- 450 mmHg2 vs. 198 +/- 22 mmHg2, p < 0.01). Furthermore, the frequency distribution in aortic stenosis was biased towards higher frequencies (mean frequency 35 +/- 14 Hz vs 54 +/- 2 Hz, p < 0.001). Turbulence intensity in aortic stenosis demonstrated beat to beat modulation by left ventricular function. The total spectral power of a sinus beat was 1888 +/- 762 mmHg2, and fell to 137 +/- 63 mmHg2 in a weak premature beat, and rose to 3618 +/- 1178 mmHg2 in a potentiated post- extrasystolic beat (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

How to cite: O'Toole, M. F., Carroll, J. D., & Feldman, T. (1993). Turbulence intensity in aortic stenosis: frequency characteristics and effects of alterations in left ventricular function. The Journal of heart valve disease, 2(1), 94–102.

Congenital obstruction of the left ventricular outflow tract remains a significant problem. Obstruction may involve the subvalvar, valvar or supravalvar portion of the aortic valve complex. Congenital valvar stenosis presenting in the neonatal period represents a spectrum of disorders ranging from the hypoplastic left heart syndrome to almost normal hearts. Preoperative echocardiography may allow the selection of infants who are suitable for biventricular repair, with the therapeutic options including open valvotomy and balloon valvotomy, but the determination of the optimal method of treatment will require long term follow up data. Subvalvar obstruction may be discrete or diffuse, and the extent will determine the appropriate therapy. Discrete membranes may be managed by a simple excision while diffuse involvement of the subvalvar region may require a more extensive reconstructive procedure such as the Konno procedure. Supravalvar aortic stenosis is the least common form of aortic stenosis and may be associated with abnormalities of the pulmonary arteries. Treatment is often palliative rather than corrective with all types of congenital left ventricular outflow tract obstruction, and many patients will require reoperations, especially those with valvar and subvalvar obstruction. The lack of long term follow up data for patients treated in the neonatal period makes the choice of an optimal therapy difficult. New methods of valve replacement such as the pulmonary autograft may improve long term results.

How to cite: Gaynor, J. W., & Elliott, M. J. (1993). Congenital left ventricular outflow tract obstruction. The Journal of heart valve disease, 2(1), 80–93.

Obstruction within the outflow tract from the left ventricle can take several anatomic forms. To understand better these substrates, we reviewed the anatomy in the normal heart and, with this background, focused on the malformations observed at each level of the outflow tract which produce stenosis. We examined 75 malformed hearts and reviewed the literature pertinent to surgical aspects of obstruction. Close study of the normal aortic valve shows the lack of any discrete fibrous structure which can be described in terms of a ring-like annulus. The semilunar attachment of the leaflets makes a crown-shaped arrangement at the ventriculo-arterial junction rather than a strict ring. In the pathological study, valvar abnormalities were found in 45 cases. The valve had three leaflets in 20 cases, two leaflets in 24 cases and one leaflet in to the other. In two cases, additional obstruction was found at the sinutubular junction. Subvalvar stenosis was found in 30 hearts, the aortic valve being trifoliate in 28 and bifoliate in 2. The main substrate of subvalvar obstruction was posterior malalignament of the outlet septum (40%), followed by muscular septal hypertrophy (23%); obstruction was also an intrinsic feature in association with atrioventricular septal defects (14%). Although rare in our material, it can also be due to a fibrous or fibromuscular shelf. In our review of the literature, we have highlighted the various forms of valvar malformation and commented on the surgical options. Clear analysis of both the level of obstruction, and its precise anatomic substrate are essential for optimal surgical intervention.

How to cite: Maizza, A. F., Ho, S. Y., & Anderson, R. H. (1993). Obstruction of the left ventricular outflow tract: anatomical observations and surgical implications. The Journal of heart valve disease, 2(1), 66–79.

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How to cite: Ross D. N. (1993). Left ventricular outflow tract: some lessons learned. The Journal of heart valve disease, 2(1), 63–65.

All oral anticoagulants act by producing a functional deficiency of vitamin K, thereby impairing the normal synthesis of factors II, VII, IX and X. All, except dicumarol, are well absorbed after oral administration. They are highly protein bound and are mainly metabolized in the liver. A number of factors such as altered absorption, distribution, elimination, genetic factors, aging, vitamin K excess or deficiency, alterations in the level of vitamin K-dependent coagulation factors and drug interactions may affect response to oral anticoagulants. Adverse effects include hemorrhage, skin necrosis and teratogenicity. Phenindione can also cause serious hypersensitivity reactions. Five oral anticoagulants are available in Europe, although warfarin, phenprocoumon and nicoumalone (acenocumarol) are the most commonly used agents. The choice of oral anticoagulant is often influenced by previous experience and familiarity, but in a survey of 22 clinical pharmacologists in 12 countries of Europe, warfarin (57%) or phenprocoumon (24%) were the agents recommended most often in clinical practice.

How to cite: Shetty, H. G., Woods, F., & Routledge, P. A. (1993). The pharmacology of oral anticoagulants: implications for therapy. The Journal of heart valve disease, 2(1), 53–62.

The prothrombin time (PT) test is the primary measurement in the laboratory control of oral anticoagulant treatment. The traditional expression of PT test results, either as percentage prothrombin activity or PT ratio, is inadequate for international communication and comparison because the values depend on the nature of the thromboplastin test system used. The WHO recommended universal scale of reporting PT results is based on calibration of local thromboplastin systems against an international reference preparation. This scale is the International Normalized Ratio (INR). Application of the INR scale in clinical practice should be encouraged by External Quality Assessment (EQA) schemes, which improve its precision. Many physicians are insufficiently aware of the different sensitivities of rabbit thromboplastins, which result in different anticoagulation intensities being employed in different clinics. Improvement in the situation can only be achieved by continuous education. The more widespread use of the INR scale should facilitate international comparison of anticoagulation results and eventually consensus on optimal target values. The introduction of the INR to countries not already using it, particularly the USA, should be strongly encouraged by all physicians with an interest in anticoagulation and especially those undertaking the long-term management of patients with prosthetic heart valves.

How to cite: van den Besselaar A. M. (1993). International standardization of laboratory control of oral anticoagulant therapy: a survey of thromboplastin reagents used for prothrombin time testing. The Journal of heart valve disease, 2(1), 42–52.

Embolic events, particularly involving the central nervous system, represent one of the important hazards associated with the implantation of mechanical valves. The use of the transcranial Doppler to insonate the middle cerebral artery has allowed us to detect microembolic events in some of these patients. Patients with long term implantation and frequent microemboli appear to be more prone to transient ischemic attacks or stroke. Evaluation of 26 patients with mechanical valves revealed 14 with detectable microemboli, four of whom experienced central nervous system symptoms. Modifications in the medical or anticoagulant regimes have not been successful in decreasing or eliminating these microemboli. As the transcranial Doppler is a non-invasive means of quantifying these microemboli, it may become a useful tool in identifying those patients in need of a new type of antithrombotic regimen, or even a valve replacement. Transcranial Doppler could thus provide advance warning before a catastrophic cerebral embolism occurs.

How to cite: Rams, J. J., Davis, D. A., Lolley, D. M., Berger, M. P., & Spencer, M. (1993). Detection of microemboli in patients with artificial heart valves using transcranial Doppler: preliminary observations. The Journal of heart valve disease, 2(1), 37–41.

The relationship between a hypercoagulable state and intracardiac thrombus formation is reviewed, with reference to the pathophysiology of intracardiac thrombus in patients with acute cardioembolic stroke, and those with mitral stenosis. When the development or enlargement of intracardiac thrombus is followed serially by echocardiography, the diameter of the inferior vena cava is seen to decrease as the hematocrit increases, particularly in patients with negative water balance taking diuretics. These findings strongly suggest that dehydration could play an important role in the formation of thrombus. A hypercoagulable and secondarily enhanced fibrinolytic state exists in the cardiac chamber of patients with acute cardioembolic stroke or with intracardiac thrombus. This can be evaluated by plasma levels of fibrinopeptide A, fibrinopeptide B beta 15-42, thrombin-antithrombin III complex and D-dimer. Anticoagulant treatment suppresses thrombin activity in the cardiac chamber, allowing plasma fibrinolytic activity to predominate and reduce the size of the intracardiac thrombus.

How to cite: Yasaka, M., & Beppu, S. (1993). Hypercoagulability in the left atrium: Part II: Coagulation factors. The Journal of heart valve disease, 2(1), 25–36.

Approximately 15% of patients with mitral valve disease will experience left atrial thrombosis and its consequences. The etiology and diagnosis of left atrial thrombosis are reviewed, stressing the importance of blood stagnation as the most important etiologic factor. Atrial fibrillation, a left atrial diameter greater than 60 mm and absence of significant mitral regurgitation are predictors of left atrial thrombosis in mitral stenosis. Left atrial thrombus can be detected in 50% of patients with all three factors; all influence blood stagnation. Smoke-like echoes in the left atrium, detected by echocardiography, provide a semi-quantitative assessment of left atrial blood stagnation. The incidence of thrombi in patients with well marked smoke-like echoes is 60%, while in those without this echocardiographic finding it is only 9%. Smoke-like echoes provide an early warning system of conditions in the left atrium likely to lead to thrombosis unless the patient is anticoagulated.

How to cite: Beppu S. (1993). Hypercoagulability in the left atrium: Part I: Echocardiography. The Journal of heart valve disease, 2(1), 18–24.

A major complication associated with prosthetic heart valves is valve thrombosis and embolization. Depending on the valve design these complications should be almost eliminated by anticoagulants or aspirin. However, valve thrombosis and embolism may occur despite apparently adequate anticoagulation. The question is whether these thrombi arise as a result of local factors such as the foreign surface and disturbance of flow at the valve site, or as a result of alteration of the hemostatic balance within the blood favoring thrombus formation. Such a disturbance, known as hypercoagulability, is the result of increased platelet activation or coagulation, or diminished fibrinolytic activity. In this article the underlying mechanism of the coagulation and fibrinolytic mechanisms is discussed, with particular emphasis on the pathways, by which activation of the coagulation system or an increase in the inhibition of fibrinolysis might occur. The laboratory tests which might be useful in detecting platelet activation, activation of coagulation or fibrinolytic activity are discussed. The potential significance of raised blood viscosity associated with a rise in fibrinogen is emphasized, in particular the fact that elevated fibrinogen is a risk marker of many types of occlusive vascular disease. Whether raised fibrinogen is causal in the pathogenesis of thrombosis at the valve site, or merely is a consequence of the prosthesis, is not known. There is some information on the fact that patients with intracardiac, and left atrial thrombi in atrial fibrillation, have activation of coagulation as shown by elevated levels of markers and also raised von Willebrand factor levels. However, it is emphasized that large scale prospective studies, in which the risk markers are measured, and then the patients with prosthetic valves followed to determine whether or not they experience clinical embolic events has not been carried out. It is unlikely that a single hemostatic test, or indeed, a number of tests, will be able to predict with accuracy the individual who is at particular risk of embolism. Nevertheless, it is important that we seek to gain further information of the mechanisms of prosthetic valve thrombus formation, and then apply this knowledge in controlled clinical trials. Only this way will better anticoagulant and antithrombotic control of these devastating embolic events be achieved.

How to cite: Gough, S. C., & Prentice, C. R. (1993). The investigation of a heart valve patient with suspected hypercoagulability. The Journal of heart valve disease, 2(1), 7–17.

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How to cite: Butchart E. G. (1993). Thrombogenesis and anticoagulation in heart valve disease: towards a rational approach. The Journal of heart valve disease, 2(1), 1–6.