Hypertension, Left Ventricular Hypertrophy, Ventricular Ectopy, and Sudden Death FRANZ
H.
MESSERLI,
M.D.,
AND FEDERICO
SORIA,
M.D.,
NewOr/eans,
Left ventricular hypertrophy (LVH) is a common sequela of sustained arterial hypertension, although the correlation between spot blood pressure measurements and LV mass is not a close one. LVH has been shown to be a powerful blood pressure-independent risk factor for cardiovascular morbidity and mortality. LVH has been shown to trigger or to accelerate ventricular dysrhythmias, although the connection between ventricular dysrhythmias and sudden death is poorly documented. LVH can be reduced by specific antihypertensive therapy; however, not all drugs are equipotent in this regard. A reduction of LVH has been shown to be associated with a suppression of ventricular dysrhythmias. Preliminary studies also indicate that the reduction of LVH may reduce its inherent excessive morbidity and mortality.
From the Department of Internal Medicine, Sectlon on Hypertension, Ochsner Clinic and Alton Ochsner MedIcal Foundation, New Orleans, Louisiana. Requests for reprints should be addressed to Franz H. Messerlr, M.D., Ochsner Clinic. 1514 Jefferson Highway, New Orleans, Louislana 70121. These data have also been presented In Drugs 1992; 44(Suppl.l):141-146.
Louisiana
A
variety of studies over the past decade have identified left ventricular hypertrophy (LVH) as a powerful risk factor for cardiovascular morbidity and mortality [1,2] (Figure 1). Since left ventricular structure can easily be assessed at the bedside and is amenable to pharmacologic intervention, LVH has evolved as a surrogate end point that potentially is more closely related to cardiovascular morbid events than is arterial pressure. This article attempts to analyze the pathophysiologic chain leading from hypertension to LVH, ventricular dysrhythmias, and ultimately to sudden death and other cardiovascular morbidity and mortality (Table I).
LEFT VENTRICULARHYPERTROPHY LVH and Hypertension Hemodynamic burden remains the single most powerful determinant of LV structure [5]. Thus, a sustained elevation of arterial pressure will invariably lead to LVH, predominantly of the concentric type, i.e., wall thickening at the expense of chamber volume. A recent study raised the question whether LVH could precede the development of hypertension [6,‘7]. Indeed, the hypertrophogenic process is modified by genetic factors [8,9], sex [lo], race 1111, age [121, and body habitus [131. Conversely, exogenous determinants such as dietary salt intake [14] and alcohol [15] also may influence the development of LVH (Figure 2). Furthermore, neurohumoral factors such as the activity of the sympathetic nervous system [16,1’7], the reninangiotensin-aldosterone cascade [M-20], and growth hormone [21], thyroid hormone [22], and insulin [231 have been documented to play a permissive if not a pathogenetic role. Given this multifactorial pathogenesis of LVH, it is hardly surprising that the correlation between spot blood pressure measurements and left ventricular (LV) mass has been documented to be poor [24]. On the other hand, 24-hour blood pressure measurements reflecting the pressure load throughout a 24-hour cycle correlate somewhat better with LV mass than casual blood pressure measurements [25]. Indeed, a recent review of this topic showed a closer correlation between 24-hour blood pressures and LV mass than between casual blood pressure and LV mass in every instance [26].
August 31, 1992
The American Journal of Medune
Volume 93 (Suppl 2A)
2A-21s
TABLE I The Pathologic Sequelae of Left Ventricular Hypertrophy 0 Decreases LV relaxabon and complrance [diminishingleft ventricular filling) * Predisposes to ventricular dysrhythmras (increasmg risk of sudden death!) l Predisposes to myocardial rschemia (increasing risk of myocardial infarction) * tong-standing LVHleads to fall in LV contractility (increasing risk of congestive heart failure) tapted from 141.
TABLE II Prevalence of Atrial and Ventricular Premature Contractions in Normotensives and in Hypettensives With and Without LVH Hypertensive Normotensive APW24 hour
1.08 + 1.78
WCs/24 hour Mean heart rate (beats/min)
8.17? 20.1 77f. 3.0
Without LVH
With LVH
1.0c 1.5 10.0? 22.1 75k 2.6
9.3c 25 475k 852; 74? 3.6
‘c = atrial premature contractions; VPC = ventricular premature contractions. ean f 1 standard deviation. I
H.
MESSERLI,
M.D.,
AND FEDERICO
SORIA,
M.D.,
NewOr/eans,
Left ventricular hypertrophy (LVH) is a common sequela of sustained arterial hypertension, although the correlation between spot blood pressure measurements and LV mass is not a close one. LVH has been shown to be a powerful blood pressure-independent risk factor for cardiovascular morbidity and mortality. LVH has been shown to trigger or to accelerate ventricular dysrhythmias, although the connection between ventricular dysrhythmias and sudden death is poorly documented. LVH can be reduced by specific antihypertensive therapy; however, not all drugs are equipotent in this regard. A reduction of LVH has been shown to be associated with a suppression of ventricular dysrhythmias. Preliminary studies also indicate that the reduction of LVH may reduce its inherent excessive morbidity and mortality.
From the Department of Internal Medicine, Sectlon on Hypertension, Ochsner Clinic and Alton Ochsner MedIcal Foundation, New Orleans, Louisiana. Requests for reprints should be addressed to Franz H. Messerlr, M.D., Ochsner Clinic. 1514 Jefferson Highway, New Orleans, Louislana 70121. These data have also been presented In Drugs 1992; 44(Suppl.l):141-146.
Louisiana
A
variety of studies over the past decade have identified left ventricular hypertrophy (LVH) as a powerful risk factor for cardiovascular morbidity and mortality [1,2] (Figure 1). Since left ventricular structure can easily be assessed at the bedside and is amenable to pharmacologic intervention, LVH has evolved as a surrogate end point that potentially is more closely related to cardiovascular morbid events than is arterial pressure. This article attempts to analyze the pathophysiologic chain leading from hypertension to LVH, ventricular dysrhythmias, and ultimately to sudden death and other cardiovascular morbidity and mortality (Table I).
LEFT VENTRICULARHYPERTROPHY LVH and Hypertension Hemodynamic burden remains the single most powerful determinant of LV structure [5]. Thus, a sustained elevation of arterial pressure will invariably lead to LVH, predominantly of the concentric type, i.e., wall thickening at the expense of chamber volume. A recent study raised the question whether LVH could precede the development of hypertension [6,‘7]. Indeed, the hypertrophogenic process is modified by genetic factors [8,9], sex [lo], race 1111, age [121, and body habitus [131. Conversely, exogenous determinants such as dietary salt intake [14] and alcohol [15] also may influence the development of LVH (Figure 2). Furthermore, neurohumoral factors such as the activity of the sympathetic nervous system [16,1’7], the reninangiotensin-aldosterone cascade [M-20], and growth hormone [21], thyroid hormone [22], and insulin [231 have been documented to play a permissive if not a pathogenetic role. Given this multifactorial pathogenesis of LVH, it is hardly surprising that the correlation between spot blood pressure measurements and left ventricular (LV) mass has been documented to be poor [24]. On the other hand, 24-hour blood pressure measurements reflecting the pressure load throughout a 24-hour cycle correlate somewhat better with LV mass than casual blood pressure measurements [25]. Indeed, a recent review of this topic showed a closer correlation between 24-hour blood pressures and LV mass than between casual blood pressure and LV mass in every instance [26].
August 31, 1992
The American Journal of Medune
Volume 93 (Suppl 2A)
2A-21s
TABLE I The Pathologic Sequelae of Left Ventricular Hypertrophy 0 Decreases LV relaxabon and complrance [diminishingleft ventricular filling) * Predisposes to ventricular dysrhythmras (increasmg risk of sudden death!) l Predisposes to myocardial rschemia (increasing risk of myocardial infarction) * tong-standing LVHleads to fall in LV contractility (increasing risk of congestive heart failure) tapted from 141.
TABLE II Prevalence of Atrial and Ventricular Premature Contractions in Normotensives and in Hypettensives With and Without LVH Hypertensive Normotensive APW24 hour
1.08 + 1.78
WCs/24 hour Mean heart rate (beats/min)
8.17? 20.1 77f. 3.0
Without LVH
With LVH
1.0c 1.5 10.0? 22.1 75k 2.6
9.3c 25 475k 852; 74? 3.6
‘c = atrial premature contractions; VPC = ventricular premature contractions. ean f 1 standard deviation. I
![[Arterial hypertension, left ventricular hypertrophy and sudden cardiac death].](/assets/img/hold.png)
