BACKGROUND: Epidemiological studies have shown that hypertension and left ventricular hypertrophy (LVH) increase the risk of sudden cardiac death (SCD) in patients with severe coronary artery disease (CAD). However, autopsy studies comparing the morphological substrates for SCD in normotensives and hypertensives are lacking. METHODS AND RESULTS: Heart weight and coronary plaque morphology were prospectively compared in SCD in 36 hypertensive and 63 normotensive individuals. The frequency of CAD was similar in hypertensives (69%, n = 25) and normotensives (73%, n = 46). In 71 hearts with CAD, acute coronary thrombi were present in 76% of normotensives versus 36% of hypertensives (P = .002), LVH was present in 64% of hypertensives versus 33% of normotensives (P = .01) and in 72% of hypertensives with one-vessel disease versus 17% of normotensives with one-vessel disease (P = .0005), and a healed or acute infarct without acute thrombus was present in 36% of hypertensives versus 9% of normotensives (P = .007). Heart weight was higher in all cases of plaque rupture (519 +/- 109 g) than eroded plaque (381 +/- 92 g, P = .0002). In contrast to hypertensives, normotensive hearts with severe CAD showed a stepwise increase in heart weight with one-, two-, and three-vessel disease (P = .01). CONCLUSIONS: Severe CAD is present in most SCD in hypertensive and normotensive individuals, but acute thrombi are more common in normotensives. LVH is an important contributing mechanism of SCD in hypertensives, especially in cases of one-vessel disease. LVH is associated with plaque rupture and extent of disease in SCD in normotensives with severe CAD.
BACKGROUND: Epidemiological studies have shown that hypertension and left ventricular hypertrophy (LVH) increase the risk of sudden cardiac death (SCD) in patients with severe coronary artery disease (CAD). However, autopsy studies comparing the morphological substrates for SCD in normotensives and hypertensives are lacking. METHODS AND RESULTS: Heart weight and coronary plaque morphology were prospectively compared in SCD in 36 hypertensive and 63 normotensive individuals. The frequency of CAD was similar in hypertensives (69%, n = 25) and normotensives (73%, n = 46). In 71 hearts with CAD, acute coronary thrombi were present in 76% of normotensives versus 36% of hypertensives (P = .002), LVH was present in 64% of hypertensives versus 33% of normotensives (P = .01) and in 72% of hypertensives with one-vessel disease versus 17% of normotensives with one-vessel disease (P = .0005), and a healed or acute infarct without acute thrombus was present in 36% of hypertensives versus 9% of normotensives (P = .007). Heart weight was higher in all cases of plaque rupture (519 +/- 109 g) than eroded plaque (381 +/- 92 g, P = .0002). In contrast to hypertensives, normotensive hearts with severe CAD showed a stepwise increase in heart weight with one-, two-, and three-vessel disease (P = .01). CONCLUSIONS: Severe CAD is present in most SCD in hypertensive and normotensive individuals, but acute thrombi are more common in normotensives. LVH is an important contributing mechanism of SCD in hypertensives, especially in cases of one-vessel disease. LVH is associated with plaque rupture and extent of disease in SCD in normotensives with severe CAD.
Authors: Daniel A Steinhaus; Eric Vittinghoff; Ellen Moffatt; Amy P Hart; Philip Ursell; Zian H Tseng Journal: Am Heart J Date: 2012-01 Impact factor: 4.749
Authors: Jari A Laukkanen; Hassan Khan; Sudhir Kurl; Peter Willeit; Jouni Karppi; Kimmo Ronkainen; Emanuele Di Angelantonio Journal: J Am Heart Assoc Date: 2014-11-05 Impact factor: 5.501
Authors: Denise L Smith; Jeannie M Haller; Maria Korre; Patricia C Fehling; Konstantina Sampani; Luiz Guilherme Grossi Porto; Costas A Christophi; Stefanos N Kales Journal: J Am Heart Assoc Date: 2018-09-18 Impact factor: 5.501