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Open Journal of Cardiology & Heart Diseases

Monitoring Cardiovascular Disease Progression

Jay N Cohn* and Mahfouz El Shahawy

University of Minnesota Medical School and Sarasota Memorial Hospital, USA

*Corresponding author: Cohn JN, University of Minnesota Medical School and Sarasota Memorial Hospital, USA

Submission: August 19, 2019;Published: August 28, 2019

DOI: 10.31031/OJCHD.2019.03.000552

ISSN 2578-0204
Volume3 Issue1

Background

Cardiovascular disease management guidelines and therapeutic trials are traditionally driven by efforts to reduce morbid events over a finite period of time, often the 10-year outcome that forms the basis for most algorithms aimed at defining risk [1,2]. This relatively short interval in a person’s life mandates that trials focus on advanced disease with high shortterm morbidity that will make it possible to identify a favorable effect of an intervention. This restriction makes it impractical to study early disease, when an intervention might be dramatically effective in prolonging life but will have too few morbid events over 5 or 10-year period of time to demonstrate effectiveness of therapy.

A proposed solution to this problem is to aim therapy not exclusively at morbidity reduction but rather at disease progression which should be a forerunner of morbid events. We have been utilizing a non-invasive evaluation program in our centers in Minneapolis, MN and Sarasota, FL over the past 20 years (Minneapolis) and 10 years (Sarasota) in order to identify early disease in need of treatment and to track disease severity to monitor progression. Our experience has convinced us that early vascular or cardiac disease detection is of great value in detecting, monitoring and treating cardiovascular disease [3].

Methodology

The goal of early detection is to identify functional and structural abnormalities of the arterial vasculature and left ventricle which identify early disease that may progress to future morbid events [4,5]. The tests of function and structure we utilize are noninvasive and non-radiating and can be completed in one room in one hour. They are aimed at detecting abnormalities of the small microvascular arteries, the large conduit arteries and the left ventricle. The underlying concept is that most cardiovascular morbid events are complications of structural or functional abnormalities in these organ systems.

The tests include the following 10 measurements [5]: 1. Resting, sitting blood pressure; 2. Pulse-contour analysis to calculate small artery compliance [6]; 3. Pulse-contour analysis to calculate large artery compliance [6]; 4. Optic fundus photography to evaluate the microvasculature; 5. Carotid ultrasound to evaluate wall thickness and plaque formation; 6. Urine specimen for microalbumin/creatinine ratio; 7. Blood pressure response to 3-minutes of mild treadmill exercise; 8. An electrocardiogram; 9. Left ventricular ultrasound for LV mass and chamber dimension; 10. A blood sample for NT-pro BNP. All 10 tests are individually graded as normal (0), borderline (+1) and abnormal (+2), with age and gender adjustment for ultrasound measurements. Both centers noted that using the total score of the 10 tests of 0-2, 3-5 and 6+ divided the population into nearly equal one-thirds. Therefore, those subgroups have been identified, respectively, as no disease, early disease and advanced disease.

Morbid events vs. disease progression

Most morbid events themselves may be precipitated by dramatic complications of cardiovascular disease, such as clots, ruptures or cardiac rhythm disorders. Nevertheless, these complications occur in the setting of advanced functional or structural abnormalities of the arteries or left ventricle. Preliminary outcome data demonstrate that those individuals without structural or functional abnormalities have a very low incidence of future morbid events and that the severity of the abnormalities is directly related to the future risk [6]. The clinical experience in this referred or self-referred asymptomatic adults in our two separate populations demonstrate that about one-third are free of abnormalities, onethird have mild or early abnormalities and one-third advanced abnormalities. If the latter subgroup were placed on preventive therapy, we might be treating one-third of the adult population, which would be consistent with the data on cardiovascular morbid events in the American population. These data raise the possibility that disease progression might serve as a substitute for morbid events to test the effectiveness of therapy aimed at preventing morbid events in an asymptomatic population.

Effect of therapy

The traditional approach to documenting the efficacy of therapy is to mount a large prospective trial powered to demonstrate a significant reduction in morbid events, over an interval long enough for adequate morbid events, to occur so that the intervention group can be demonstrated to have fewer events than the non-intervention group. This approach has required studying populations with a high near-term risk of a morbid event. If disease progression could be utilized as a substitute for events, far smaller trials over shorter intervals in individuals with early disease might be possible.

We have undertaken three intervention trials of drug therapy in the early stage of disease that provides encouraging evidence that such an approach is feasible [7-9]. This approach needs further documentation so that regulatory bodies may accept disease progression as a suitable endpoint for effectiveness. Such a result would open the door for improved management of the early stages of cardiovascular disease and a population-wide prolongation of healthy life.

References

  1. D Agostino RB, Vasan RS, Pencina MJ, Wolf PA, Cobain M, et al. (2008) General cardiovascular risk profile for use in primary care: the Framingham heart study. Circulation 117(6): 743-753.
  2. Goff DC Jr, Lloyd-Jones DM, Bennett G, Coady S, D'Agostino RB, et al. (2014) 2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American college of cardiology/American heart association task force on practice guidelines. Circulation 129(25 Suppl 2): S49-73.
  3. Duprez DA, Florea N, Zhong W, Grandits GA, Hawthorne CK, et al. (2011) Vascular and cardiac functional and structural screening to identify risk of future morbid events: preliminary observations. J Am Soc Hypertens 5(5): 401-409.
  4. North BJ, Sinclair DA (2012) The intersection between aging and cardiovascular disease. Circ Res 110(8): 1097-1108.
  5. Lakatta EG, Levy D (2003) Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: Part I: aging arteries: a "set up" for vascular disease. Circulation 107(1): 139-146.
  6. Den Ruijter HM, Peters SA, Anderson TJ, Britton AR, Dekker JM, et al. (2012) Common carotid intima-media thickness measurements in cardiovascular risk prediction: a meta-analysis. JAMA 308(8): 796-803.
  7. Duprez DA, Florea ND, Jones K, Cohn JN (2007) Beneficial effects of valsartan in asymptomatic individuals with vascular or cardiac abnormalities: the DETECTIV pilot study. J Am Coll Cardiol 50(9): 835-839.
  8. Saul SM, Duprez DA, Zhong W, Grandits GA, Cohn JN (2013) Effect of carvedilol, lisinopril and their combination on vascular and cardiac health in patients with borderline blood pressure: the detect study. J Hum Hypertens 27(6): 362-367.
  9. Duprez DA, Florea N, Duval S, Koukol C, Cohn JN (2017) Effect of nebivolol or atenolol vs. placebo on cardiovascular health in subjects with borderline blood pressure: the evidence study. J Hum Hypertens 32(1): 20-25.

© 2019 Cohn JN. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and build upon your work non-commercially.



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